What the Board expects you to know:
- The divisions of the nervous system: central and peripheral (somatic and autonomic).
- The structure and function of sensory, relay and motor neurons. The process of synaptic transmission, including reference to neurotransmitters, excitation and inhibition.
- The function of the endocrine system: glands and hormones.
- The fight or flight response including the role of adrenaline.
- Localisation of function in the brain and hemispheric lateralisation: motor, somatosensory, visual, auditory and language centres; Broca’s and Wernicke’s areas, split brain research. Plasticity and functional recovery of the brain after trauma.
- Ways of studying the brain: scanning techniques, including functional magnetic resonance imaging (fMRI); electroencephalogram (EEGs) and event-related potentials (ERPs); post-mortem examinations.
- Biological rhythms: circadian, infradian and ultradian and the difference between these rhythms. The effect of endogenous pacemakers and exogenous zeitgebers on the sleep/wake cycle.
Communication Systems in the Body
The body has two main systems of communication, one fast and precise the other slower with a more global effect. As we shall see, the two systems do work well together.
Nervous System
Is the main system of communication in the body. It receives information from the environment, processes information and allows us to respond accordingly. It also acts to coordinate the working of organs, tissues and cells within the body. It can be sub-divided into the following sections:
The body has two main systems of communication, one fast and precise the other slower with a more global effect. As we shall see, the two systems do work well together.
Nervous System
Is the main system of communication in the body. It receives information from the environment, processes information and allows us to respond accordingly. It also acts to coordinate the working of organs, tissues and cells within the body. It can be sub-divided into the following sections:
Central Nervous System
The CNS consists of the brain and spinal cord. All but the most basic creatures on Earth share a similar set up, however, the brains of primates and in particular humans has become incredibly sophisticated and is what sets us apart from all other species. We shall look at the human brain in more detail later.
The spinal cord is the brain’s extension into the rest of the body, allowing communication with the peripheral nervous system.
Peripheral Nervous System (PNS)
The PNS allows communication between the CNS and our internal and external environment. It carries message to and from all organs and tissues as well the external world via our senses. This can be sub-divided into:
Somatic Nervous System (SNS)
Carries message from the senses and allows conscious control of our muscles via motor neurons.
Autonomic Nervous System (ANS)
Controls all the functions of the body over which we have no or little conscious control such as breathing, digestion, respiration and, as we shall see later, our stress response.
The Endocrine System
The endocrine or hormonal system is the second system of communication within the body and is finely coordinated with the nervous system.
It is comprised of a number of glands located around the body that secrete a variety of hormones. Hormones are proteins that have a powerful effect on the organs they target. For example adrenaline stimulates beta receptors on the surface of the heart causing it to beat harder and faster. Hormones are transported around the body in the bloodstream so there are able to affect large parts of the body at any one time if needed.
Gland |
Hormone(s) |
Function |
Testes |
Testosterone |
Production of male reproductive system and secondary sex characteristics |
Ovaries |
Oestrogen, progesterone... |
Development of female sexual characteristics. Maintains pregnancy |
Adrenal |
Adrenaline, noradrenaline, cortisol |
Controls body’s response to stress by increasing heart rate and energy available. Increases blood sugar levels and helps cope with longer term stress |
Pineal |
Melatonin |
Sleep hormone |
Pituitary |
Growth hormone, oxytocin |
Promotes growth and repair Regulates child birth and breastfeeding |
|
The glands of the body are controlled by the pituitary (master) gland that is located just beneath the hypothalamus in the brain. It secretes a number of hormones that have specific effects on the body such as growth hormone or that directly influence the function of other glands such as ACTH that stimulates the adrenal cortex trigging it to produce cortisol.
In turn the pituitary gland is controlled by the hypothalamus that regulates many vital functions with the body such as biological rhythms, eating behaviour and our response to stress. Hormones are involved in all of these functions. |
|
Working together: ANS and Endocrine System
The body’s reaction to stress is old fashioned. In the modern World, in the vast majority of stress situations the body’s response to stress causes more harm than good. However, in the olden days, like tens or hundreds of thousands of years ago, our present day response to stress would have been a lifesaver.
Faced with danger such as a sabre-tooth tiger or a warring tribe down the road then a sudden mobilisation of energy in the body was useful. Consider the typical response to stress:
- Increased heart rate
- Increased blood pressure
- Relaxation of the lung’s bronchi (air channels widen)
- Release of glucose into the blood
- Dilation of pupils (letting more light into the eye)
- Slowing of digestion (allowing blood to flow to muscles, heart etc).
This is referred to as the 3fs response (fright: flight or fight) and serves a simple purpose. It is pumping oxygen and glucose around the body providing energy to the areas where it’s most needed. If the danger persists we can fight or we can turn and run. If danger passes then very quickly the body can return to normal and primitive man can return to taking Dino for a walk!
The important bits
The hypothalamus controls the body’s response to stress. This is situated right next to the pituitary gland (sometimes referred to as the master gland because it controls the others) and both are located in the middle of the brain just behind the upper part of your nose!
In the stress response the Pituitary gland does two things.
- It sends nerve messages to the adrenal medulla (part of the adrenal gland)
- It sends a chemical ACTH to the adrenal cortex (another part of the adrenal gland).
Triggers the sympathetic nervous system and releases adrenaline.
This produces the 3Fs response:
- Increased heart rate
- Slows digestion
- Dilates pupils
- Releases glucose into blood…
Releases steroids into bloodstream
This causes:
- Liver to release glucose
- Inhibits immune response especially inflammation and production of white blood cells.
- Convert fats/proteins into glucose.
|
SAM (sympathetico adrenal medullary)
Call it by its Christian name by all means, but the full name does explain what is involved. It is a sympathetic response in that it creates arousal and activity within the brain and body and it involves the adrenal medulla. On first becoming aware of a stressor the hypothalamus activates the sympathetic branch of the ANS. Noradrenaline is released to all parts of the body but specifically messages are sent via neurons to the adrenal medulla. Remember: FIREMAN SAM for a FAST response. The adrenal medulla secretes adrenaline which in turn produces the 3fs response: Increased alertness (e.g. dilation of pupils) Increased flow of blood to the muscles and the brain Increased respiration to provide muscles and brain with more oxygen In addition, there is a slowing of digestion and increased circulation of blood clotting factors in case of injury. Because of the electrical mediation of the message from brain to adrenal gland this all happens within the blinking of an eye. In fact, it has been shown to swing into action before we become consciously aware of the potential threat. |
HPA (Hypothalamic Pituitary Adrenal)
This is a much slower response, designed for dealing with the effects of longer term, chronic stress. The end product (cortisol) is often referred to as the stress hormone.
The HPA is not designed with immediate safety in mind but is there to help the body cope with the longer term consequences of stress and also the punishing effects of the SAM response. Here goes:
- The higher centres of the brain (cortex) become aware of stress or danger. These pass the message on to the hypothalamus which controls the endocrine or hormonal system of the body.
- The hypothalamus releases a chemical CRF (cortico-trophin releasing factor) which stimulates the pituitary gland into action.
- The anterior lobe of the pituitary gland now secretes a hormone called ACTH (adreno-cortico trophic hormone).
- ACTH acts on the adrenal cortex (as the name suggests) causing it to secrete cortisol.
Cortisol results in
- Release of energy (glycogen)
- Lowered sensitivity to pain
- Lowered immune response
- Impaired cognitive functions such as concentration
- Slowing of digestion
The whole process reaches a peak after about 20 minutes of the initial stressor.
Finally on the biology: Don’t forget the parasympathetic response!
Once the stress is over the body has to return to normal. Heart rate and blood pressure drop back to resting levels, blood glucose is converted back into glycogen for storage, the immune and digestive systems return to pre-stress levels of functioning.
Beware the question that provides a scenario of a short-lived stress that quickly disappears. This would entail a SAM (sympathetic response) but quickly replaced by the parasympathetic response.
Evaluation of the Physiological Model
This is clearly a very biological approach to stress. It only considers events inside the body and sees stress as a purely physical response. It does not consider differences between people, for example why one person’s stress is another person’s pleasure.
Mason (1975) measured the levels of adrenaline produced by stressors in different people. The same stressors produce different levels of adrenaline in different people depending on how they interpret the stress. The physiological model does not consider people’s interpretations or perceptions of stress.
People without adrenal glands die when stressed unless they receive injections of cortisol (a steroid). They have to be given training in avoiding or minimising stress!
Once the stress is over the body has to return to normal. Heart rate and blood pressure drop back to resting levels, blood glucose is converted back into glycogen for storage, the immune and digestive systems return to pre-stress levels of functioning.
Beware the question that provides a scenario of a short-lived stress that quickly disappears. This would entail a SAM (sympathetic response) but quickly replaced by the parasympathetic response.
Evaluation of the Physiological Model
This is clearly a very biological approach to stress. It only considers events inside the body and sees stress as a purely physical response. It does not consider differences between people, for example why one person’s stress is another person’s pleasure.
Mason (1975) measured the levels of adrenaline produced by stressors in different people. The same stressors produce different levels of adrenaline in different people depending on how they interpret the stress. The physiological model does not consider people’s interpretations or perceptions of stress.
People without adrenal glands die when stressed unless they receive injections of cortisol (a steroid). They have to be given training in avoiding or minimising stress!
The Neuron
The building blocks of the nervous system. It is estimated that there are 100billion neurons in the human nervous system, most of which are located in the brain.
They come in three main flavours: sensory, relay(interneuron) and motor.
Component |
Function |
Cell body (soma) |
Play no part in transmission of the nervous impulse. It acts as a factory providing the proteins and energy needed by the neuron. |
Nucleus |
Contains the genetic material of the cell. |
Dendrites |
Receive chemical signals from other neurons that can then be converted into electrical impulses. |
Axon |
Carries the impulse from the cell body and along the neuron. |
Myelin Sheath |
A fatty layer that acts as insulation and speeds up the transmission. It gives white matter of the brain it’s distinctive lighter colour. |
Nodes of Ranvier |
Gaps in the myelin that allows the action potential to jump from node to node and speed up transmission even more. |
Terminal buttons |
These are at the end of the axon and allow communication with the dendrites of neighbouring neurons. |
Generating an action potential
Action potentials are caused when different ions cross the neuron membrane. A stimulus first causes sodium channels to open. Because there are many more sodium ions (with a positive charge) on the outside, and the inside of the neuron is negative relative to the outside, sodium ions rush into the neuron. This causes the inside of the cell to become positive for a fraction of a second. This creates the action potential that is then propagated along the axon.
The Synapse
This is the gap between adjoining neurons. For a message to be passed from one neuron to the next it must cross the synaptic cleft. (Note: strictle speaking the synapse includes the pre-synaptic terminal and the receptor sites on the post-synaptic side.
The synapse brings flexibility to the flow of information. At the synapse the ‘decision’ is made whether to continue the message or whether to block it. All drugs, prescription or recreational, have their effect at the synapse by manipulating this basic process in some way.
Action potentials are caused when different ions cross the neuron membrane. A stimulus first causes sodium channels to open. Because there are many more sodium ions (with a positive charge) on the outside, and the inside of the neuron is negative relative to the outside, sodium ions rush into the neuron. This causes the inside of the cell to become positive for a fraction of a second. This creates the action potential that is then propagated along the axon.
The Synapse
This is the gap between adjoining neurons. For a message to be passed from one neuron to the next it must cross the synaptic cleft. (Note: strictle speaking the synapse includes the pre-synaptic terminal and the receptor sites on the post-synaptic side.
- An action potential reaches the pre-synaptic terminal
- Calcium channels open and calcium ions flow into the pre-synaptic terminal
- This causes vesicles filled with a neurotransmitter to migrate to the outer membrane
- The vesicles spill their contents into the synaptic cleft.
- The neurotransmitters released cross the synaptic cleft.
- The neurotransmitter binds with receptors on the post synaptic site.
- This affects the permeability of the membrane and can then trigger an action potential in the next neuron.
- Any unused neurotransmitter is recycled through reuptake channels on the presynaptic side. The vesicles can then be restocked ready for the next action potential.
The synapse brings flexibility to the flow of information. At the synapse the ‘decision’ is made whether to continue the message or whether to block it. All drugs, prescription or recreational, have their effect at the synapse by manipulating this basic process in some way.
Excitation and Inhibition (The Ying and Yang of neural pathways)
These two processes are key to the proper functioning of your nervous system. Put simply, excitation of the post-synaptic neuron makes it more likely that it will fire and inhibition makes it less likely. The latter will effectively block the signal and the information being carried will go no further.
I’m sure we all agree that neurotransmitters are sexy chemicals and I’m sure you all have your favourites: dopamine and serotonin are almost certainly up there with acetyl choline and adrenaline probably coming in third and fourth. After all, these are the chemicals of choice when it comes to pleasure, excitement, eating and sleeping and cravings. Not many people would include glutamate and GABA in their top five.
In fact it’s unlikely that many A-level psychology students have ever heard of glutamate, or if they have assumed it was a food additive designed to make you salivate when you have takeaway. However, these are probably the most important neurotransmitters in the brain.
When released at the synapse, glutamate has an excitatory effect and GABA an inhibitory. A brain dominated by glutamate would be in a constant state of exciting itself with unrestrained bursts of activity. Sounds like fun but in effect would be like one massive non-stop epileptic seizure. One dominated by GABA would be comatose with little in the way of communication. A healthy E/I balance is now recognised as an important measure of brain fitness.
A low E/I is associated with schizophrenia caused by a weak glutamate system. Autism on the other hand is associated with a high E/I and linked to a weak GABA system. Apparently autistic patients are far more prone to epileptic seizures as a result of this lack of inhibition in the nervous system.
For background interest or extension only
Below: The ways in which drugs can affect the synapse with some examples of each
These two processes are key to the proper functioning of your nervous system. Put simply, excitation of the post-synaptic neuron makes it more likely that it will fire and inhibition makes it less likely. The latter will effectively block the signal and the information being carried will go no further.
I’m sure we all agree that neurotransmitters are sexy chemicals and I’m sure you all have your favourites: dopamine and serotonin are almost certainly up there with acetyl choline and adrenaline probably coming in third and fourth. After all, these are the chemicals of choice when it comes to pleasure, excitement, eating and sleeping and cravings. Not many people would include glutamate and GABA in their top five.
In fact it’s unlikely that many A-level psychology students have ever heard of glutamate, or if they have assumed it was a food additive designed to make you salivate when you have takeaway. However, these are probably the most important neurotransmitters in the brain.
When released at the synapse, glutamate has an excitatory effect and GABA an inhibitory. A brain dominated by glutamate would be in a constant state of exciting itself with unrestrained bursts of activity. Sounds like fun but in effect would be like one massive non-stop epileptic seizure. One dominated by GABA would be comatose with little in the way of communication. A healthy E/I balance is now recognised as an important measure of brain fitness.
A low E/I is associated with schizophrenia caused by a weak glutamate system. Autism on the other hand is associated with a high E/I and linked to a weak GABA system. Apparently autistic patients are far more prone to epileptic seizures as a result of this lack of inhibition in the nervous system.
For background interest or extension only
Below: The ways in which drugs can affect the synapse with some examples of each
The Cerebral Cortex
Picture a typical brain and what you have in your mind is mostly cerebral cortex; that heavily creased and grooved outer layer of the brain. This is the most modern part of the brain and in evolutionary terms, a relative newcomer. The cortex is sometimes referred to as grey matter because of its colour. The neurons in this part of the brain, all 10 to 15 billion of them, lack myelin sheath so appear grey in colour. The cortex is only 2 to 5 mm thick but comprises the largest part of the cerebrum and about 65% of the total mass of the brain.
The cortex is clearly divided into two hemispheres, more on that later. Each hemisphere is sub-divided into four functionally distinct lobes, each getting their name from the area of cranium that sits over their top.
Areas the Board expect you to know about:
1. Frontal lobe
No prizes for guessing where you’ll find this. It can loosely be split into two areas:
Pre-Frontal Cortex or PFC
This area at the very front of the brain is responsible for executive functions such as planning, problem solving, reasoning and impulse control (link to addiction). The central executive of the working memory model lives in the PFC. Phineas Gage suffered severe damage to this area and lost the ability to plan and to focus his attention. This area also plays a role in personality.
Further back in the frontal lobe is the primary motor cortex that has direct links with the spinal cord and allows us to control voluntary movement of the body.
Motor Cortex
A strip of the cortex lying immediately anterior to the central sulcus. This area of the brain controls voluntary movement of the body and was first mapped by the great Wilder Penfield during his research on epileptic volunteers. As with all things-brain-related it appears to have an inverse image of the body. When Penfield electrically stimulated areas of the motor cortex, corresponding areas of the body would be seen to move.
No prizes for guessing where you’ll find this. It can loosely be split into two areas:
Pre-Frontal Cortex or PFC
This area at the very front of the brain is responsible for executive functions such as planning, problem solving, reasoning and impulse control (link to addiction). The central executive of the working memory model lives in the PFC. Phineas Gage suffered severe damage to this area and lost the ability to plan and to focus his attention. This area also plays a role in personality.
Further back in the frontal lobe is the primary motor cortex that has direct links with the spinal cord and allows us to control voluntary movement of the body.
Motor Cortex
A strip of the cortex lying immediately anterior to the central sulcus. This area of the brain controls voluntary movement of the body and was first mapped by the great Wilder Penfield during his research on epileptic volunteers. As with all things-brain-related it appears to have an inverse image of the body. When Penfield electrically stimulated areas of the motor cortex, corresponding areas of the body would be seen to move.
2. Parietal Lobe
The parietal lobe is separated from the frontal lobe by the central sulcus. It’s main feature is the somatosensory cortex (pictured above and to the right). The somatosensory cortex is very similar in structure to the motor cortex but receives input from the senses rather than sending output to the muscles. It too has an inverted layout with areas at the top controlling the lower limbs and areas at the bottom controlling the head, especially tongue, noses, lips and eyes.
When Penfield stimulated different parts of the somatosensory cortex in conscious patients they would experience sensations in the corresponding body parts.
3. Occipital Lobe
This lies at the back of the brain just above the cerebellum. It contains the primary visual cortex responsible for the receiving and interpretation of visual information. Again it is organised so that the left lobe receives information from the right visual field of each eye and the right lobe from the left visual field of each eye. More on this when we look at Sperry’s research on split brain patients. Damage, say to the left primary visual cortex can result in blindness in the right visual field of both eyes.
Language centres
In the mid to late nineteenth century two researchers, working independently isolated two brain areas that ever since have been linked with specific aspects of language:
Paul Broca, whilst working on a patient, forever referred to as Tan discovered a brain area seemingly responsible for production of speech. Tan could produce one word (you guessed it ‘Tan’). On Tan’s death, a post-mortem revealed damage to an area in the rear portion of the temporal lobe, now known as Broca’s Area. Broca’s Aphasia results in slowed and very limited speech.
A few years later Karl Wernicke reported a condition in which speech production is fine, but they struggle to comprehend language and the speech they produce is meaningless. On their death post-mortems revealed damage to an area further back in the temporal lobe, forever after referred to as Wernicke’s Area. Wernicke’s Aphasia is a condition resulting in the production of nonsense and meaningless words (neologisms). See Donald Trump!
4. Temporal Lobe
This is associated with receiving and interpreting auditory information but also in the associated task of understanding and producing language. Note: the section above on language areas, although still required by the Board and still a favourite of text books has now been shown to be so overly simplified it barely holds any truth at all!
Evidence and Evaluation
Clearly this whole area is very scientific and awash with carefully controlled, objective measures for isolating specific brain areas and measuring associated functions. fMRI scans can be used to show that Broca’s and Wenicke’s areas are active during certain tasks.
Neurosurgery
Our early understanding of brain function was gained almost entirely from patients with cognitive deficiencies, much like those observed by Broca and Wernicke. By the twentieth century this was being supplemented by evidence from the increasing number of surgical procedures being carried out on the brain. Psychosurgery, in which healthy tissue was removed from the brain in order to change behaviour, taught us the importance of the frontal lobes of the brain. Early attempts pioneered by Walter Freeman were haphazard and involved the disconnection of the frontal lobes from the rest of the brain.
Later in the century, as our understanding improved, techniques were refined. Unfortunately not in time to help HM of course. William Scoville’s removal of HM’s hippocampus (on both sides) resulted in a catastrophic inability to create new long term memories, but made it apparent what the role of the hippocampus was… more evidence for localisation of function.
Modern day neurosurgery is more precise and considered. Removal of the cingulate gyrus of the limbic system, known to be involved in pain, emotional responses and the reduction and avoidance of negative consequences has led to improvement in the symptoms of some patients with OCD. Dougherty et al (2002): out of 44 patients who had undergone the procedure, a third showed significant improvement after eight months with a further 14% showing partial improvement. Again this can be used as evidence for localisation as it does suggest that specific brain areas might be serving a specific function.
Evidence Against
Karl Lashley provided a huge amount of information invaluable in the early days of neuroscience. In the 1940s and 50s he carried out surgical procedures on hundreds of animals, mostly rats. His research was vital to our later understanding of eating behaviour, pain and pleasure. However, he did find that removal of anything up to 50% of a rat’s brain had no impact on its ability to learn and to run a maze. This suggests that learning is not isolated to one specific brain areas but does appear to be more globally organised, requiring the involvement of most of the brain. A far more holistic concept, more in keeping with nineteenth century thinking.
Similarly, the next section on plasticity, the idea that the brain can reorganise or rewire itself in order to recover function if one area has been damaged. This suggests that localisation of function can be re-written or at least isn’t as fixed as the initial theory predicts.
Phineas Gage
In 1848, Gage, 25, was the foreman of a crew cutting a railroad bed in Cavendish, Vermont. On September 13, as he was using a tamping iron to pack explosive powder into a hole, the powder detonated. The tamping iron—43 inches long, 1.25 inches in diameter and weighing 13.25 pounds—shot skyward, penetrated Gage’s left cheek, ripped into his brain and exited through his skull, landing several dozen feet away. Though blinded in his left eye, he might not even have lost consciousness, and he remained savvy enough to tell a doctor that day, “Here is business enough for you.”
Amazingly Phineas survived the accident and in fact lived on for another eleven years. However, he was never quite the same man. His personality changed and he became more aggressive and prone to bouts of extreme profanity. Friends reported that he ‘was no longer Gage.’ He could no longer hold down a steady job, being unable to concentrate or focus his attention. This gave vital clues to the function of the pre-frontal cortex, damaged by the accident. We now know it is the home of the central executive (WMM), responsible for organizing STM and our ability to solve problems, switch attention and plan effectively.
Phineas spent the rest of his life as a circus freak show artist; people paying to see the man with a hole in his head.
The parietal lobe is separated from the frontal lobe by the central sulcus. It’s main feature is the somatosensory cortex (pictured above and to the right). The somatosensory cortex is very similar in structure to the motor cortex but receives input from the senses rather than sending output to the muscles. It too has an inverted layout with areas at the top controlling the lower limbs and areas at the bottom controlling the head, especially tongue, noses, lips and eyes.
When Penfield stimulated different parts of the somatosensory cortex in conscious patients they would experience sensations in the corresponding body parts.
3. Occipital Lobe
This lies at the back of the brain just above the cerebellum. It contains the primary visual cortex responsible for the receiving and interpretation of visual information. Again it is organised so that the left lobe receives information from the right visual field of each eye and the right lobe from the left visual field of each eye. More on this when we look at Sperry’s research on split brain patients. Damage, say to the left primary visual cortex can result in blindness in the right visual field of both eyes.
Language centres
In the mid to late nineteenth century two researchers, working independently isolated two brain areas that ever since have been linked with specific aspects of language:
Paul Broca, whilst working on a patient, forever referred to as Tan discovered a brain area seemingly responsible for production of speech. Tan could produce one word (you guessed it ‘Tan’). On Tan’s death, a post-mortem revealed damage to an area in the rear portion of the temporal lobe, now known as Broca’s Area. Broca’s Aphasia results in slowed and very limited speech.
A few years later Karl Wernicke reported a condition in which speech production is fine, but they struggle to comprehend language and the speech they produce is meaningless. On their death post-mortems revealed damage to an area further back in the temporal lobe, forever after referred to as Wernicke’s Area. Wernicke’s Aphasia is a condition resulting in the production of nonsense and meaningless words (neologisms). See Donald Trump!
4. Temporal Lobe
This is associated with receiving and interpreting auditory information but also in the associated task of understanding and producing language. Note: the section above on language areas, although still required by the Board and still a favourite of text books has now been shown to be so overly simplified it barely holds any truth at all!
Evidence and Evaluation
Clearly this whole area is very scientific and awash with carefully controlled, objective measures for isolating specific brain areas and measuring associated functions. fMRI scans can be used to show that Broca’s and Wenicke’s areas are active during certain tasks.
Neurosurgery
Our early understanding of brain function was gained almost entirely from patients with cognitive deficiencies, much like those observed by Broca and Wernicke. By the twentieth century this was being supplemented by evidence from the increasing number of surgical procedures being carried out on the brain. Psychosurgery, in which healthy tissue was removed from the brain in order to change behaviour, taught us the importance of the frontal lobes of the brain. Early attempts pioneered by Walter Freeman were haphazard and involved the disconnection of the frontal lobes from the rest of the brain.
Later in the century, as our understanding improved, techniques were refined. Unfortunately not in time to help HM of course. William Scoville’s removal of HM’s hippocampus (on both sides) resulted in a catastrophic inability to create new long term memories, but made it apparent what the role of the hippocampus was… more evidence for localisation of function.
Modern day neurosurgery is more precise and considered. Removal of the cingulate gyrus of the limbic system, known to be involved in pain, emotional responses and the reduction and avoidance of negative consequences has led to improvement in the symptoms of some patients with OCD. Dougherty et al (2002): out of 44 patients who had undergone the procedure, a third showed significant improvement after eight months with a further 14% showing partial improvement. Again this can be used as evidence for localisation as it does suggest that specific brain areas might be serving a specific function.
Evidence Against
Karl Lashley provided a huge amount of information invaluable in the early days of neuroscience. In the 1940s and 50s he carried out surgical procedures on hundreds of animals, mostly rats. His research was vital to our later understanding of eating behaviour, pain and pleasure. However, he did find that removal of anything up to 50% of a rat’s brain had no impact on its ability to learn and to run a maze. This suggests that learning is not isolated to one specific brain areas but does appear to be more globally organised, requiring the involvement of most of the brain. A far more holistic concept, more in keeping with nineteenth century thinking.
Similarly, the next section on plasticity, the idea that the brain can reorganise or rewire itself in order to recover function if one area has been damaged. This suggests that localisation of function can be re-written or at least isn’t as fixed as the initial theory predicts.
Phineas Gage
In 1848, Gage, 25, was the foreman of a crew cutting a railroad bed in Cavendish, Vermont. On September 13, as he was using a tamping iron to pack explosive powder into a hole, the powder detonated. The tamping iron—43 inches long, 1.25 inches in diameter and weighing 13.25 pounds—shot skyward, penetrated Gage’s left cheek, ripped into his brain and exited through his skull, landing several dozen feet away. Though blinded in his left eye, he might not even have lost consciousness, and he remained savvy enough to tell a doctor that day, “Here is business enough for you.”
Amazingly Phineas survived the accident and in fact lived on for another eleven years. However, he was never quite the same man. His personality changed and he became more aggressive and prone to bouts of extreme profanity. Friends reported that he ‘was no longer Gage.’ He could no longer hold down a steady job, being unable to concentrate or focus his attention. This gave vital clues to the function of the pre-frontal cortex, damaged by the accident. We now know it is the home of the central executive (WMM), responsible for organizing STM and our ability to solve problems, switch attention and plan effectively.
Phineas spent the rest of his life as a circus freak show artist; people paying to see the man with a hole in his head.
Plasticity and Functional Recovery
Plasticity
The brain has a certain capacity to be flexible. Throughout life it continues to make new connections. Each of its one billion neurons can create up to 10,000 synaptic connections. It is estimated that the average human brain has over one trillion such connections but in fact the actual figure may be ten times this. Such is difficulty in accurately measuring brain systems. This process doesn’t stop in childhood, as it used to be thought, but continues throughout life, although there may be a peak in early childhood. Later in life, little-used neural connections may be lost, a process known as synaptic pruning.
London taxi drivers in the process of learning The Knowledge show an increased density in the grey matter of their hippocampi, known to be involved in memory and certainly in other species, is spatial memory. Racing pigeons show a similar growth in their hippocampi which is thought to be involved in remembering locations, enabling them to home.
Other brain structures show similar growth. Draganski et al (2006) carried out a natural experiment on German medical students three months prior to their exams and again immediately afterwards. The researchers found changes in their hippocampi and in the parietal cortex, known to be involved in learning. Think about using your research methods here. Natural experiment so high in external validity, the independent variable has occurred due to a naturally occurring real event. However, lack of control over other variables may also be important, stress, changes in sleeping and eating habits etc. As a result, cause and effect relationships are difficult to establish.
Plastic changes also occur in musicians brains compared to non-musicians. Gaser and Schlaug (2003) compared professional musicians (who practice at least 1hour per day) to amateur musicians and non-musicians. They found that gray matter (cortex) volume was highest in professional musicians, intermediate in amateur musicians, and lowest in non-musicians in several brain areas involved in playing music: motor regions, anterior superior parietal areas and inferior temporal areas.
Functional recovery
This is neural plasticity of a different type, the ability of the brain to recover function following a trauma such as stroke or period of drug abuse. Areas left unaffected and can sometimes take over the function of areas that have been damaged. This can be a very rapid process. Although the process isn’t fully understood, it seems new synaptic connections can be formed that that effectively bypass the damaged area. Similar to building a new bridge between two areas after the original one has been washed away.
Strictly speaking recovery of function occurs in two phases following a stroke or similar damage:
Neurological recovery, dependent on the brain damage that has occurred
Functional recovery, dependent on motivation and environmental factors.
Structural changes can include:
- Axonal sprouting: the formation of new pathways by developing new nerve endings that can connect to neighbouring undamaged neurons (see bridge analogy above).
- Reformation of blood cells: essential for oxygen supply and glucose.
- Recruitment of similar areas. For example a similar structure in the other hemisphere.
Phantom Limb Pain (when plasticity goes bad)
One theory of phantom limb pain suggests it’s due to brain plasticity that has gone wrong. Following the loss of the limb, the brain area responsible for sensation in that limb becomes vacant. It’s no longer receiving sensory input.
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Other parts of the body may then take over this area and send their sensory input to the vacant area. However, the brain is unaware of this and assumes this new input must still be coming from the lost limb. The result is sensations in a part of the body that no longer exists.
Recently developed mirror therapy has proved beneficial in the treatment of some phantom limb patients. |
Extension
However, recent research by Makin at Oxford University has cast doubt on this theory. Using functional magnetic resonance imaging (fMRI), which measures changes in blood flow due to brain activity, Makin's (2013) scanned the brains of hand amputees, two-armed individuals, and people born with only one hand. As the participants were being scanned, they were told to move their hands, arms, feet or lips. Amputees with phantom pain were told to perform the movements with their phantom limb, whereas amputees with no phantom pain and those born without a hand were told to simply imagine moving their hand or arm. [The 9 Most Bizarre Medical Conditions]
The scans showed that amputees with phantom pain had the same pattern of brain activity as individuals with both hands. This was a huge surprise, Makin said. "If we take an individual who suffers from phantom pain, his brain would be indistinguishable from your brain."
Practical Applications
As the process has become better understood, neurologists have developed techniques that can aid the process. Typically, recovery of function slows after a few weeks. Neurorehabilitation now involves using techniques such as electrical stimulation to continue the process after it has slowed.
Not surprisingly, much like the body, the brain becomes less plastic with age and is less able to recover function following trauma. However, our knowledge of plasticity has now developed cognitive tasks for the elderly that can slow down deterioration of cognitive functions as the brain ages. Bezzola et al (2012) used fMRI scans to show that 40 hours of golf training to show increased neural representation of movement in areas of the motor cortex in middle-aged participants. (Middle aged being 40-60 years of age apparently L).
Cognitive reserve
The length of time a person has spent in education can impact upon recovery. The longer a person has spent in education, the greater their chance of a fuller recovery. This is referred to as their cognitive reserve.
Split-brain research
Now we consider the extent to which the two hemispheres of the brain are distinct. As we’ve already seen language is located in the left hemisphere giving the impression that the two sides may be very different. Pick up any tacky text in the ‘Pop Psychology’ selection at Waterstones and you’ll be left with the impression that you have two brains in your skull.
Split-brain patients (background information)
In the 1950s a group of patients, all of whom were experiencing epileptic seizures underwent a dramatic surgical procedure. To prevent the electrical current that causes a seizure spreading to both sides of the brain and rendering the patient unconscious, the main bundle of fibres connecting the two halves were severed. This procedure, a commissurotomy (cutting of the corpus callosum) amazingly caused few if any obvious deficits.
Two decades later, Roger Sperry carried out his Nobel Prize-winning research on eleven of these patients:
Basic procedure
Items, pictures or words are presented to either the left or the right visual field. Images presented to the right would be passed to the left hemisphere of the brain and images presented to the left would be passed to the right hemisphere.
This causes no issues in normal participants. The information in one hemisphere would immediately be passed to the other hemisphere via the corpus callosum. This isn’t possible in split-brain patients. Information in the right is stuck in the right.
Since only the left hemisphere has language ability images appearing in the right hemisphere cannot be verbalised. The right hemisphere knows what it has seen but is unable to transfer this information to the left. However, these patients are able to communicate what the right hemisphere knows by drawing the image with their left hand or by selecting a corresponding item with their left hand.
When subsequently asked why they have drawn the image, the left brain, still unaware of what the right has seen, is unable to explain.
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Composite words
In this variation, words such as keyring or football would be split and presented to different visual fields. For example, ‘key’ would be presented on the left (going to the right hemisphere) and ‘ring’ would be presented to the right (going to the left hemisphere). When asked what they had seen they would say ‘ring’ (language centres on the left. When asked to pick a matching object from behind a screen with their left hand (controlled by the right hemisphere) they would pick up a key |
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Faces
If different faces were presented to the right and left visual field and the patient then asked to choose which one they’d seen from a variety of others presented, the one presented to the left would always be chosen. This seems to suggest that the right hemisphere is dominant in facial recognition. Similarly the right appears dominant with visual images such as shapes.
Generally speaking, the right is the synthesiser, performing best on spatial and musical tasks and the left the analyser, geared up for language and mathematical skills.
Evaluation
Methodology
Sperry’s research was tightly controlled. Each participant would go through precisely the same procedure with images being presented via a tachistoscope for one tenth of a second, giving the patient no time to turn and see the image with both sides of the eyes. With such tight control of all other variables he was able to establish a cause and effect relationship between brain hemisphere and function. Such tight control also allowed for replication ensuring reliability of findings.
However, as mentioned earlier, only eleven patients were tested. Eleven people with highly abnormal brains and a history of epileptic seizures requiring drug treatment. As a result, generalising findings to the population as a whole is troublesome. Not only that but the surgical procedure wasn’t the same in each patient. Different amounts of separation had taken place. Today when the procedure is performed it is usual for the frontal two thirds of the corpus callosum to be severed. If this isn’t sufficient to elicit results, the remaining, dorsal one third is severed.
Two brains in one head?
Pucetti (1977) concluded that the two hemispheres were so different we essentially did have two brains in our skull, giving rise to that host of pop psychology. In practice, because of the sharing of information across the corpus callosum in normal brains, both sides of the brain are involved in all tasks.
Brain scanning
If different faces were presented to the right and left visual field and the patient then asked to choose which one they’d seen from a variety of others presented, the one presented to the left would always be chosen. This seems to suggest that the right hemisphere is dominant in facial recognition. Similarly the right appears dominant with visual images such as shapes.
Generally speaking, the right is the synthesiser, performing best on spatial and musical tasks and the left the analyser, geared up for language and mathematical skills.
Evaluation
Methodology
Sperry’s research was tightly controlled. Each participant would go through precisely the same procedure with images being presented via a tachistoscope for one tenth of a second, giving the patient no time to turn and see the image with both sides of the eyes. With such tight control of all other variables he was able to establish a cause and effect relationship between brain hemisphere and function. Such tight control also allowed for replication ensuring reliability of findings.
However, as mentioned earlier, only eleven patients were tested. Eleven people with highly abnormal brains and a history of epileptic seizures requiring drug treatment. As a result, generalising findings to the population as a whole is troublesome. Not only that but the surgical procedure wasn’t the same in each patient. Different amounts of separation had taken place. Today when the procedure is performed it is usual for the frontal two thirds of the corpus callosum to be severed. If this isn’t sufficient to elicit results, the remaining, dorsal one third is severed.
Two brains in one head?
Pucetti (1977) concluded that the two hemispheres were so different we essentially did have two brains in our skull, giving rise to that host of pop psychology. In practice, because of the sharing of information across the corpus callosum in normal brains, both sides of the brain are involved in all tasks.
Brain scanning
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Electroencephalogram (EEG)
Measuring brain activity, the good old-fashioned way. The EEG has been around since the 1920s and still has its uses today. It measures global electrical activity in the brain via a series of electrodes attached to the scalp. The readout produced is a measure of millions of neurons firing at any one time. Evaluation It has its uses in diagnosing some neurological conditions such as tumours and seizures. It has been vital in sleep research and provided our knowledge of the five stages of sleep. Unlike some other techniques it has high temporal resolution, the readings produced changing the moment brain activity changes (to the millisecond). However, it is unable to measure activity in precise locations within the brain. It has very poor spatial resolution. It produces a measure global electrical activity so researchers are unable to locate what brain structures are most active. |
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Event-Related Potentials (ERPs)
Modern technology allows for sophisticated filtering of the EEG. The EEG itself contains a huge amount of information about brain activity. However, in its raw form it is impossible to isolate the electrical activity from specific functions or locations. Statistical averaging software however, can filter out unwanted brain activity leaving only the ERP related to a specific function.
Evaluation
Because they are based on the EEG they have very high temporal resolution providing a millisecond by millisecond image of brain activity. They are therefore widely used in the measuring of cognitive functions and have been a useful tool in assessing cognitive deficits in brain-damaged patients. They have also been used widely in the study of conditions such as Parkinson’s, dementia and OCD.
In practice it can be difficult to eliminate all extraneous ERPs and focus on the one required.
Functional Magnetic Resonance Imaging (fMRI)
Based on the simple idea that cells that are more active, need more energy and therefore more oxygen. As a result more blood flows to these cells (haemodynamic response). The fMRI uses powerful magnetic fields to detect these changes in blood flow which in turn detects the brain areas that most active.
Evaluation
The measure is non-invasive. Unlike PET scans there are no injections, no pain and no exposure to radiation. Spatial resolution, unlike EEGs is very high. Researchers can detect the precise areas that are most active.
Unfortunately, the patient must remain totally motionless during the procedure, not always easy whilst being asked to complete cognitive tasks. Also, temporal resolution, compared to EEGs, is very poor. There can be anything up to a 5 second delay between action and detection. Although it is precise, it still cannot detect the activity of specific neurons. A weakness that has delayed research into mirror neurons.
Biological Rhythms
Introduction
Most human and non-human animal functions are cyclic, alternating over a period of time. Obvious examples include the sleep-wake cycle which repeats over a 24 hour cycle, or the hibernation patterns of some creatures that typically rest through the winter months and awaken in spring. The major debate, similar to the nature/nurture in some respects, but without the controversy, is to what extent biological rhythms are determined by internal clocks (endogenous factors) and by environmental factors (so called zeitgebers).
What has become apparent in recent years is the ancient nature of the rhythms. Clocks have been found to exist in the very simplest forms of life, algae. It therefore seems reasonable to assume that they have been around since the beginning of life on Earth. Biological rhythms allow organisms to adapt to the cycle of day and night and they appear to control nearly all behaviours and physiological processes.
In this topic we consider the three main categories of biological rhythms and the extent to which they are controlled by internal and external factors. We then consider what happens when our rhythms are disrupted.
Circadian Rhythms (about 24 hours)
Infradian Rhythms (greater than 24 hours)
Ultradian Rhythms (less than 24 hours at night)
There are others that we might mention en passant:
Circannual rhythms, as the name suggests rhythms that cycle over a period of one year. These are therefore a subset of infradian.
Diurnal rhythms that are less than 24 hours but confined to daytime or waking hours, as opposed to ultradian at night or during sleep.
Circadian
Variation is a cycle that repeats over an approximate 24 hour period. The word stems from the Latin; circa (meaning ‘about’) and diem (meaning ‘day’). There are some cycles that we are consciously aware of; the sleep/wake cycle being an obvious one, but most cycles we are not usually aware of. For example our core body temperature fluctuates over a 24 hour period. Generally it peaks mid afternoon at about 37.1 C and troughs in the wee small hours at about 36.7 C. This may not sound like a lot but you may nevertheless have noticed the effect and found yourself shivering unexpectedly as you’ve walked home after a late night party, even in August!
Other examples of human circadian rhythm include heart rate, metabolism and breathing. These follow a similar pattern to temperature, which may not seem surprising, since they match our patterns of activity. However, people on shifts, who are sleeping through the day and more active at night still keep the same circadian rhythms with body temperature, metabolism and resting heart rate still peaking mid afternoon!
Blood clotting also shows a circadian rhythm, peaking in the morning and coinciding with increased incidence of heart attack
It is worth mentioning that there are big differences between individuals. The most noticeable being the larks/owls division; larks being morning types and owls preferring the evenings. Typically when studied larks seem to be clock advanced having rhythms about two hours ahead of owls.
Modern technology allows for sophisticated filtering of the EEG. The EEG itself contains a huge amount of information about brain activity. However, in its raw form it is impossible to isolate the electrical activity from specific functions or locations. Statistical averaging software however, can filter out unwanted brain activity leaving only the ERP related to a specific function.
Evaluation
Because they are based on the EEG they have very high temporal resolution providing a millisecond by millisecond image of brain activity. They are therefore widely used in the measuring of cognitive functions and have been a useful tool in assessing cognitive deficits in brain-damaged patients. They have also been used widely in the study of conditions such as Parkinson’s, dementia and OCD.
In practice it can be difficult to eliminate all extraneous ERPs and focus on the one required.
Functional Magnetic Resonance Imaging (fMRI)
Based on the simple idea that cells that are more active, need more energy and therefore more oxygen. As a result more blood flows to these cells (haemodynamic response). The fMRI uses powerful magnetic fields to detect these changes in blood flow which in turn detects the brain areas that most active.
Evaluation
The measure is non-invasive. Unlike PET scans there are no injections, no pain and no exposure to radiation. Spatial resolution, unlike EEGs is very high. Researchers can detect the precise areas that are most active.
Unfortunately, the patient must remain totally motionless during the procedure, not always easy whilst being asked to complete cognitive tasks. Also, temporal resolution, compared to EEGs, is very poor. There can be anything up to a 5 second delay between action and detection. Although it is precise, it still cannot detect the activity of specific neurons. A weakness that has delayed research into mirror neurons.
Biological Rhythms
Introduction
Most human and non-human animal functions are cyclic, alternating over a period of time. Obvious examples include the sleep-wake cycle which repeats over a 24 hour cycle, or the hibernation patterns of some creatures that typically rest through the winter months and awaken in spring. The major debate, similar to the nature/nurture in some respects, but without the controversy, is to what extent biological rhythms are determined by internal clocks (endogenous factors) and by environmental factors (so called zeitgebers).
What has become apparent in recent years is the ancient nature of the rhythms. Clocks have been found to exist in the very simplest forms of life, algae. It therefore seems reasonable to assume that they have been around since the beginning of life on Earth. Biological rhythms allow organisms to adapt to the cycle of day and night and they appear to control nearly all behaviours and physiological processes.
In this topic we consider the three main categories of biological rhythms and the extent to which they are controlled by internal and external factors. We then consider what happens when our rhythms are disrupted.
Circadian Rhythms (about 24 hours)
Infradian Rhythms (greater than 24 hours)
Ultradian Rhythms (less than 24 hours at night)
There are others that we might mention en passant:
Circannual rhythms, as the name suggests rhythms that cycle over a period of one year. These are therefore a subset of infradian.
Diurnal rhythms that are less than 24 hours but confined to daytime or waking hours, as opposed to ultradian at night or during sleep.
Circadian
Variation is a cycle that repeats over an approximate 24 hour period. The word stems from the Latin; circa (meaning ‘about’) and diem (meaning ‘day’). There are some cycles that we are consciously aware of; the sleep/wake cycle being an obvious one, but most cycles we are not usually aware of. For example our core body temperature fluctuates over a 24 hour period. Generally it peaks mid afternoon at about 37.1 C and troughs in the wee small hours at about 36.7 C. This may not sound like a lot but you may nevertheless have noticed the effect and found yourself shivering unexpectedly as you’ve walked home after a late night party, even in August!
Other examples of human circadian rhythm include heart rate, metabolism and breathing. These follow a similar pattern to temperature, which may not seem surprising, since they match our patterns of activity. However, people on shifts, who are sleeping through the day and more active at night still keep the same circadian rhythms with body temperature, metabolism and resting heart rate still peaking mid afternoon!
Blood clotting also shows a circadian rhythm, peaking in the morning and coinciding with increased incidence of heart attack
It is worth mentioning that there are big differences between individuals. The most noticeable being the larks/owls division; larks being morning types and owls preferring the evenings. Typically when studied larks seem to be clock advanced having rhythms about two hours ahead of owls.
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Background info for interest only!
French geologist (and speleologist) Michael Siffre is the daddy! Over the past 40 years or so he has regularly spent extended periods of time in various caves around the World and agreed to be studied during the process. His first stint was in 1962 when he spent 61 days in a cave in the Alps. He emerged on September 17th but thought it was August 20th! He receives no unsolicited contact with the outside World, but does shout to co-workers at the cave entrance when he wakes, prior to sleep and before meals. In 1972 he was monitored by NASA in the caves of Texas and in 1999 he missed the millennium celebrations in a cave in some part of the World. He spent new year’s eve eating foie gras and quaffing champagne. He subsequently discovered that his celebrations were over three days late! Each time his body clock extended form the usual 24 to around 24.5 hours. Occasionally this extended to 48 hours, 36 hours awake and 12 to 14 hours asleep. |
This appears to suggest two things:
There is internal control of the circadian rhythm, since even in the absence of external cues we are able to maintain a regular daily cycle.
There must usually be some external cue that entrains this cycle to 24 hours. When this is removed we adopt this very strange 24.5 or 25 hour cycle.
Evaluation
Clearly, there are methodological issues with this case study. At the best of times it is difficult to generalise from one person and create a nomothetic theory of the human circadian sleep/wake cycle. However, we all have such different biological rhythms so it is even more difficult than usual to generalise in this case.
There is internal control of the circadian rhythm, since even in the absence of external cues we are able to maintain a regular daily cycle.
There must usually be some external cue that entrains this cycle to 24 hours. When this is removed we adopt this very strange 24.5 or 25 hour cycle.
Evaluation
Clearly, there are methodological issues with this case study. At the best of times it is difficult to generalise from one person and create a nomothetic theory of the human circadian sleep/wake cycle. However, we all have such different biological rhythms so it is even more difficult than usual to generalise in this case.
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However, there is supporting evidence. Aschoff and Wever have repeated the study many times in the Andechs Bunker in Germany. Jurgen Aschoff was in fact the original participant being studied by Rutger Wever. In the years that followed over 400 participants have volunteered to take part in their studies and in nearly all cases of isolation, with no natural light, the participants’ sleep/wake cycles extended to between 24.5 and 25 hours. Far more convincing evidence than Siffre alone.
Right: A volunteer emerging from the Anders Bunker where Aschoff and Wever conducted their research. |
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Some have criticised this research since it is so artificial. In particular they object to the use of strong artificial light by the participants. On waking the volunteers such as Siffre switch on lights which are likely to artificially re-set the body clock. Czeisler et al (1999) has argued this is the equivalent of providing powerful drugs.
In their own version, Czeisler et al kept 24 participants in constant artificial low-level light for one month and put them on a 28 hour cycle. When readings of body temperature and blood chemicals were analysed they were shown to have adopted a cycle of 24 hours and 11 minutes, much closer to the 24 hours we would expect.
Others however, disagree with Czeisler. In an attempt to find the endogenous clocks’ period volunteers have been exposed to severe variations in clock alteration, for example, exposing participants to artificial lighting simulating a 28 hour day. (So if ‘sunrise’ was at 6am on day 1 it would be at 10am on day 2 and so on). The body cannot adjust to such extremes and the body clocks ‘run free.’ In all cases the cycle is greater than the usual 24 hours but estimates vary as to the exact length. Some put the increase at as little as 11 minutes whereas others claim one hour.
Folkard (1985) showed the limitation of purely exogenous factors in controlling the rhythm. He got 12 volunteers to spend 3 weeks in isolation with no natural light. They were instructed to go to bed when the clock suggested 23.45 and set alarms for 07.45. After a few days the clock was speeded up so that the supposed 24 hours were passing in only 22. Only one of the volunteers kept pace. The other twelve all maintained a 24 hour rhythm, suggesting internal biological factors were over-riding exogenous factors (in this case quite literally ‘time-giver’ in the form of a clock!).
Recent research
It seems that most people in the industrialised world are out of synchronisation with the natural world and this might be posing all sorts of risks for our physiological and psychological health.
A recent study looked at the extent to which our natural clock might be lagging behind sunrise and sunset and how this can quickly be adjusted. A small group of volunteers were tested. It was found that most were going to sleep after midnight and that as a result their melatonin levels were still high when they woke up in the morning and often were still high two hours after waking. This meant that they were working against their natural cycles.
However, after one week’s camping in Colorado, no artificial light other than campfire allowed, their clocks were back in tune with sunrise and sunset. On average they had shifted backwards by two hours so were sleeping and rising earlier, although total sleep time had not been affected. Melatonin was being secreted earlier and levels were dropping long before waking. Crucial to this shift appeared to be natural light. It was estimated that total exposure to natural light had increased fourfold. (Wright 2013)
Practical applications of research into the body clock
Think back to the Horizon documentary using the body clock to better treat cancers and improve the psychological health of patients with Alzheimer’s. Dr Reddy’s research at the University of Cambridge (2012):
The body’s immune system is more effective at certain times of the day. For example, patients with blood poisoning are more likely to die between the hours of 2 and 6 am when the body’s defences are at their weakest.
Reddy and his co-workers have found that a protein TLR9 which detects the DNA of microbes such as bacteria and viruses is controlled by the body clock, at least in mice! Immunising mice when their body clock is at its peak is most effective in fighting off a range of infections, much as treatment with chemotherapy we saw in the video.
They have concluded that drugs need to be administered at certain times of the day perhaps longer term, drugs can be administered to alter the body clock to its optimum level.
Shift work
Major disasters such as Chernobyl and Three-mile Island, Bhopal (explosion at a chemical plant in India), Exxon Valdez (oil tanker spillage in Alaska and many other major incidents have occurred in the early hours of the morning and been attributed to tiredness. Additionally on the roads in Britain there are a disproportionately high number of fatal accidents in the early hours of the morning
In addition to accidents and disasters there are also health risks associated with regular shift work. These include increased risk of heart disease and digestive disorders and regular tiredness. Twenty percent of shift workers report falling asleep whilst at work. This clearly has implications both for safety and for productivity and efficiency.
Shifts can follow a number of patterns:
Rotating or fixed?
A rotating pattern involves working different hours each week or month. A typical three shift system covering a 24 hour period would involve people working:
Cooper et al (2005) compared rotating shift patterns with fixed. Oil rig workers on either twelve hour day shifts or twelve hour night shifts were compared to workers on a split-shift pattern (working seven days of night shifts followed by seven days of night shifts). Urine tests measuring melatonin levels showed that those on split shifts never fully synchronised. They also had significantly higher levels of circulating fatty acids putting them at greater risk of CHD and hypertension.
Fast or slow rotation?
Although most research suggests a clockwise rotation is to be preferred, there is disagreement over the speed of rotation. Czeisler (main man in this area) recommends a slow rotation, for example spending at least three weeks on each shift. Bambra (2008) however, prefers a faster rotation of just 3 to 4 days on each pattern so the body never has time to adjust to the new cycle.
Fixed shifts tend to be rarer, mostly because of the unsociable hours involved. For example working a permanent 10pm to 6am shift. Although this allows time for resynchronisation with the worked adjusting to the shift pattern it does create problems at weekends when people revert back to a normal sleep-wake pattern.
Using artificial light to reset the body clock
Boivin et al (1996) put 31 male participants on an inverted sleep pattern (so they were awake at night and slept during the day). This lasted for three days. Each day when they woke they were sat in front of dim lights for 5 hours and then placed in one of four conditions:
After three days:
Group 1 had advanced by five hours (they were adapting to the new pattern best)
Group 2 had advanced by three hours
Group 3 had advanced by one hour
Group 4 had drifted backwards by one hour (were failing to show any signs of adapting).
Conclusion
Artificial light, even ordinary room light can help us adapt our biological rhythms to suit the environment; however, brighter light is even more effective. Clearly this could be useful in the workplace to help shift workers to adapt to changing sleep-wake cycles.
In their own version, Czeisler et al kept 24 participants in constant artificial low-level light for one month and put them on a 28 hour cycle. When readings of body temperature and blood chemicals were analysed they were shown to have adopted a cycle of 24 hours and 11 minutes, much closer to the 24 hours we would expect.
Others however, disagree with Czeisler. In an attempt to find the endogenous clocks’ period volunteers have been exposed to severe variations in clock alteration, for example, exposing participants to artificial lighting simulating a 28 hour day. (So if ‘sunrise’ was at 6am on day 1 it would be at 10am on day 2 and so on). The body cannot adjust to such extremes and the body clocks ‘run free.’ In all cases the cycle is greater than the usual 24 hours but estimates vary as to the exact length. Some put the increase at as little as 11 minutes whereas others claim one hour.
Folkard (1985) showed the limitation of purely exogenous factors in controlling the rhythm. He got 12 volunteers to spend 3 weeks in isolation with no natural light. They were instructed to go to bed when the clock suggested 23.45 and set alarms for 07.45. After a few days the clock was speeded up so that the supposed 24 hours were passing in only 22. Only one of the volunteers kept pace. The other twelve all maintained a 24 hour rhythm, suggesting internal biological factors were over-riding exogenous factors (in this case quite literally ‘time-giver’ in the form of a clock!).
Recent research
It seems that most people in the industrialised world are out of synchronisation with the natural world and this might be posing all sorts of risks for our physiological and psychological health.
A recent study looked at the extent to which our natural clock might be lagging behind sunrise and sunset and how this can quickly be adjusted. A small group of volunteers were tested. It was found that most were going to sleep after midnight and that as a result their melatonin levels were still high when they woke up in the morning and often were still high two hours after waking. This meant that they were working against their natural cycles.
However, after one week’s camping in Colorado, no artificial light other than campfire allowed, their clocks were back in tune with sunrise and sunset. On average they had shifted backwards by two hours so were sleeping and rising earlier, although total sleep time had not been affected. Melatonin was being secreted earlier and levels were dropping long before waking. Crucial to this shift appeared to be natural light. It was estimated that total exposure to natural light had increased fourfold. (Wright 2013)
Practical applications of research into the body clock
Think back to the Horizon documentary using the body clock to better treat cancers and improve the psychological health of patients with Alzheimer’s. Dr Reddy’s research at the University of Cambridge (2012):
The body’s immune system is more effective at certain times of the day. For example, patients with blood poisoning are more likely to die between the hours of 2 and 6 am when the body’s defences are at their weakest.
Reddy and his co-workers have found that a protein TLR9 which detects the DNA of microbes such as bacteria and viruses is controlled by the body clock, at least in mice! Immunising mice when their body clock is at its peak is most effective in fighting off a range of infections, much as treatment with chemotherapy we saw in the video.
They have concluded that drugs need to be administered at certain times of the day perhaps longer term, drugs can be administered to alter the body clock to its optimum level.
Shift work
Major disasters such as Chernobyl and Three-mile Island, Bhopal (explosion at a chemical plant in India), Exxon Valdez (oil tanker spillage in Alaska and many other major incidents have occurred in the early hours of the morning and been attributed to tiredness. Additionally on the roads in Britain there are a disproportionately high number of fatal accidents in the early hours of the morning
In addition to accidents and disasters there are also health risks associated with regular shift work. These include increased risk of heart disease and digestive disorders and regular tiredness. Twenty percent of shift workers report falling asleep whilst at work. This clearly has implications both for safety and for productivity and efficiency.
Shifts can follow a number of patterns:
Rotating or fixed?
A rotating pattern involves working different hours each week or month. A typical three shift system covering a 24 hour period would involve people working:
- 6am to 2 pm
- 2pm to 10pm
- 10pm to 6am
Cooper et al (2005) compared rotating shift patterns with fixed. Oil rig workers on either twelve hour day shifts or twelve hour night shifts were compared to workers on a split-shift pattern (working seven days of night shifts followed by seven days of night shifts). Urine tests measuring melatonin levels showed that those on split shifts never fully synchronised. They also had significantly higher levels of circulating fatty acids putting them at greater risk of CHD and hypertension.
Fast or slow rotation?
Although most research suggests a clockwise rotation is to be preferred, there is disagreement over the speed of rotation. Czeisler (main man in this area) recommends a slow rotation, for example spending at least three weeks on each shift. Bambra (2008) however, prefers a faster rotation of just 3 to 4 days on each pattern so the body never has time to adjust to the new cycle.
Fixed shifts tend to be rarer, mostly because of the unsociable hours involved. For example working a permanent 10pm to 6am shift. Although this allows time for resynchronisation with the worked adjusting to the shift pattern it does create problems at weekends when people revert back to a normal sleep-wake pattern.
Using artificial light to reset the body clock
Boivin et al (1996) put 31 male participants on an inverted sleep pattern (so they were awake at night and slept during the day). This lasted for three days. Each day when they woke they were sat in front of dim lights for 5 hours and then placed in one of four conditions:
- Very bright light
- Bright light
- Ordinary room light
- Continued dim light
After three days:
Group 1 had advanced by five hours (they were adapting to the new pattern best)
Group 2 had advanced by three hours
Group 3 had advanced by one hour
Group 4 had drifted backwards by one hour (were failing to show any signs of adapting).
Conclusion
Artificial light, even ordinary room light can help us adapt our biological rhythms to suit the environment; however, brighter light is even more effective. Clearly this could be useful in the workplace to help shift workers to adapt to changing sleep-wake cycles.
The Ultradian Rhythm
These occur more than once in a 24 hour cycle and at night time. We shall consider the stages of sleep. As you should be aware, a typical night’s sleep takes you from stage 1 to 4 then back to 2 and finally into REM. This whole cycle then repeats itself three or four more times during the night, each cycle lasting about 90 minutes. There are a number of similar cycles during the daytime too. Sometimes these are referred to as diurnal. Examples include eating (approximately every four hours), smoking and urination.
Aserinsky and Kleitman (1957)
Nine participants were studies (seven male and two female)
Participants ate normally (excluding coffee and alcohol) then arrived at the laboratory just before their normal bedtime. They went to sleep with electrodes attached beside the eyes (EOG) and on the scalp (EEG). Participants were woken by a doorbell at various times during the night and asked to describe their dream if they were having one, then returned to sleep.
Participants were woken either in REM or NREM (but not told which). They confirmed whether they were having a dream and described the content into a recorder. The direction of eye movements was detected using electrodes around the eyes. Participants were woken after the persistence of a single eye-movement pattern for more than one minute and asked to report their dream. The eye-movement patterns were either: mainly vertical, mainly horizontal, both vertical and horizontal, very little or no movement.
Findings:
Uninterrupted dream stages lasted 3-50 minutes (mean approx 20 minutes), were typically longer later in the night and showed intermittent bursts of around 2-100 REMs.
The cycle length varied between participants but was consistent within individuals, eg 70 for one, 104 for another. When woken in NREM participants returned to NREM, but when woken in REM they typically didn’t dream again until the next REM phase (except sometimes in the final REM phase).
Participants frequently described dreams when woken in REM but rarely did so from NREM sleep (although there were some individual differences) and this differences was marked at the end of the NREM period (within 8 minutes of cessation of REM – only 6 dreams recalled in 132 awakenings). In NREM awakenings, participants tended to describe feelings but not specific dream content.
Accuracy of estimation of 5 or 15 minutes’ of REM was very high (88% and 78% respectively). REM duration and number of words in the narrative were significantly positively correlated. Eye movement patterns were related to dream content, eg horizontal movements in a dream about throwing tomatoes, vertical ones in a dream about ladders and few movements in dreams about staring fixedly at something.
Conclusion:
Dreaming is reported from REM but not nREM sleep, participants can judge the length of their dream duration and REM patterns relate to dream content.
Evaluation
As with most sleep research, sample size is very smalln making generalisations difficult, particularly when there are such great individual differences between participants.
Sleep laboratories are very artificial settings. The participants’ pre-sleep routine is very different to at home, they are in unfamiliar surroundings and covered with a plethora of electrodes and wires. They also know that they’re being observed.
However, sleep studies like this do allow for physiological measurements which are objective and replicable. Unfortunately self-report techniques are just the opposite, subjective and non-verifiable. Given the fragile nature of dreams self report of these must be seen as particularly unreliable.
These occur more than once in a 24 hour cycle and at night time. We shall consider the stages of sleep. As you should be aware, a typical night’s sleep takes you from stage 1 to 4 then back to 2 and finally into REM. This whole cycle then repeats itself three or four more times during the night, each cycle lasting about 90 minutes. There are a number of similar cycles during the daytime too. Sometimes these are referred to as diurnal. Examples include eating (approximately every four hours), smoking and urination.
Aserinsky and Kleitman (1957)
Nine participants were studies (seven male and two female)
Participants ate normally (excluding coffee and alcohol) then arrived at the laboratory just before their normal bedtime. They went to sleep with electrodes attached beside the eyes (EOG) and on the scalp (EEG). Participants were woken by a doorbell at various times during the night and asked to describe their dream if they were having one, then returned to sleep.
Participants were woken either in REM or NREM (but not told which). They confirmed whether they were having a dream and described the content into a recorder. The direction of eye movements was detected using electrodes around the eyes. Participants were woken after the persistence of a single eye-movement pattern for more than one minute and asked to report their dream. The eye-movement patterns were either: mainly vertical, mainly horizontal, both vertical and horizontal, very little or no movement.
Findings:
Uninterrupted dream stages lasted 3-50 minutes (mean approx 20 minutes), were typically longer later in the night and showed intermittent bursts of around 2-100 REMs.
The cycle length varied between participants but was consistent within individuals, eg 70 for one, 104 for another. When woken in NREM participants returned to NREM, but when woken in REM they typically didn’t dream again until the next REM phase (except sometimes in the final REM phase).
Participants frequently described dreams when woken in REM but rarely did so from NREM sleep (although there were some individual differences) and this differences was marked at the end of the NREM period (within 8 minutes of cessation of REM – only 6 dreams recalled in 132 awakenings). In NREM awakenings, participants tended to describe feelings but not specific dream content.
Accuracy of estimation of 5 or 15 minutes’ of REM was very high (88% and 78% respectively). REM duration and number of words in the narrative were significantly positively correlated. Eye movement patterns were related to dream content, eg horizontal movements in a dream about throwing tomatoes, vertical ones in a dream about ladders and few movements in dreams about staring fixedly at something.
Conclusion:
Dreaming is reported from REM but not nREM sleep, participants can judge the length of their dream duration and REM patterns relate to dream content.
Evaluation
As with most sleep research, sample size is very smalln making generalisations difficult, particularly when there are such great individual differences between participants.
Sleep laboratories are very artificial settings. The participants’ pre-sleep routine is very different to at home, they are in unfamiliar surroundings and covered with a plethora of electrodes and wires. They also know that they’re being observed.
However, sleep studies like this do allow for physiological measurements which are objective and replicable. Unfortunately self-report techniques are just the opposite, subjective and non-verifiable. Given the fragile nature of dreams self report of these must be seen as particularly unreliable.
Awake
The brain is obviously active and shows what is called beta activity (see EEG above). When we relax, for example close our eyes or meditate the brain shows alpha activity.
Stage 1 sleep (15 minutes)
This occurs at the start of a nights sleep. It lasts a matter of minutes and you will all be familiar with it since we often wake from this stage. For example sat watching ‘Big Brother’ gradually losing the will to live or certainly to stay awake, we may nod off. We may wake from this stage and think that we’ve been dreaming. In fact these hallucinations are referred to as hypnogogic phenomena and usually comprise fleeting images rather than the bizarre stories more characteristic of dreaming. The eyes may roll slowly. Sometimes we may wake without realising that we’ve even nodded off. Brain waves are slower and are called ‘theta.’ Other times we may wake with a jerk or knee twitch.
Stage 2 sleep (20 minutes)
After about a minute or so we enter stage 2. This is characterised by bursts of high frequency waves called ‘sleep spindles.’ We are still aware of sounds and activity around us and the brain responds to this with K-complexes. We are still very easily woken.
Stage 3 sleep (15 minutes)
The brain waves start to slow and become higher in amplitude and wavelength. These are called delta waves and are associated with deep sleep. We are now more difficult to wake. First time round in the night this stage is brief, only a few minutes, but we spend longer in it later in the night.
Stage 4 sleep (30 minutes)
In many respects this is a continuation of stage 4, however, delta waves now constitute most of the brain activity and we are now at our most relaxed. At this stage we are very difficult to wake up and even vigorous shaking may not be sufficient to wake some people, me included. However, a quiet but meaningful sound such as a baby crying can be sufficient, again indicating that the brain still retains some degree of awareness to external stimuli! Heart rate and blood pressure fall, muscles are very relaxed and temperature is at its lowest.
REM sleep (10 minutes at start of night, up to an hour later in the night)
Sometimes referred to rather unimaginatively as stage 5, or more descriptively ‘paradoxical sleep.’ REM is strange. The brain now becomes very active, almost indistinguishable from a waking brain. Remember the activation-synthesis theory of dreaming? The pons in the midbrain throws out bursts of electrical activity into the cortex lighting it up like a Christmas tree. Heart rate and blood pressure increase, as does body temperature, and the eyes twitch rapidly giving this stage its name. But, despite this frantic activity the body remains motionless, cut off from the brain by the pons. We are paralysed and unable to act out the brain’s bizarre thoughts.
REM is now thought by some to be the deepest stage of sleep since it is now that we are most difficult to wake up. However, this could be as a result of being so absorbed in our dreams.
Paralysis appears to be to prevent the body acting out our dreams and endangering our lives. Cats that have had lesions to the pons do in fact appear to act out their dreams. Remember, however, that we have no certain way of knowing whether lower species do dream; it is merely assumed that they do because all warm blooded creatures (birds and mammals), with the exception of the very early egg-laying mammals, have REM sleep.
Our first visit to REM typically lasts about for about 10 minutes and we start our journey back down to stage 2, stage 3 and stage 4 sleep. This cycle repeats throughout the night, however, as the diagram below illustrates, we spend most of the first half of the night in deep sleep (slow wave or NREM), and most of the second half in REM sleep.
The brain is obviously active and shows what is called beta activity (see EEG above). When we relax, for example close our eyes or meditate the brain shows alpha activity.
Stage 1 sleep (15 minutes)
This occurs at the start of a nights sleep. It lasts a matter of minutes and you will all be familiar with it since we often wake from this stage. For example sat watching ‘Big Brother’ gradually losing the will to live or certainly to stay awake, we may nod off. We may wake from this stage and think that we’ve been dreaming. In fact these hallucinations are referred to as hypnogogic phenomena and usually comprise fleeting images rather than the bizarre stories more characteristic of dreaming. The eyes may roll slowly. Sometimes we may wake without realising that we’ve even nodded off. Brain waves are slower and are called ‘theta.’ Other times we may wake with a jerk or knee twitch.
Stage 2 sleep (20 minutes)
After about a minute or so we enter stage 2. This is characterised by bursts of high frequency waves called ‘sleep spindles.’ We are still aware of sounds and activity around us and the brain responds to this with K-complexes. We are still very easily woken.
Stage 3 sleep (15 minutes)
The brain waves start to slow and become higher in amplitude and wavelength. These are called delta waves and are associated with deep sleep. We are now more difficult to wake. First time round in the night this stage is brief, only a few minutes, but we spend longer in it later in the night.
Stage 4 sleep (30 minutes)
In many respects this is a continuation of stage 4, however, delta waves now constitute most of the brain activity and we are now at our most relaxed. At this stage we are very difficult to wake up and even vigorous shaking may not be sufficient to wake some people, me included. However, a quiet but meaningful sound such as a baby crying can be sufficient, again indicating that the brain still retains some degree of awareness to external stimuli! Heart rate and blood pressure fall, muscles are very relaxed and temperature is at its lowest.
REM sleep (10 minutes at start of night, up to an hour later in the night)
Sometimes referred to rather unimaginatively as stage 5, or more descriptively ‘paradoxical sleep.’ REM is strange. The brain now becomes very active, almost indistinguishable from a waking brain. Remember the activation-synthesis theory of dreaming? The pons in the midbrain throws out bursts of electrical activity into the cortex lighting it up like a Christmas tree. Heart rate and blood pressure increase, as does body temperature, and the eyes twitch rapidly giving this stage its name. But, despite this frantic activity the body remains motionless, cut off from the brain by the pons. We are paralysed and unable to act out the brain’s bizarre thoughts.
REM is now thought by some to be the deepest stage of sleep since it is now that we are most difficult to wake up. However, this could be as a result of being so absorbed in our dreams.
Paralysis appears to be to prevent the body acting out our dreams and endangering our lives. Cats that have had lesions to the pons do in fact appear to act out their dreams. Remember, however, that we have no certain way of knowing whether lower species do dream; it is merely assumed that they do because all warm blooded creatures (birds and mammals), with the exception of the very early egg-laying mammals, have REM sleep.
Our first visit to REM typically lasts about for about 10 minutes and we start our journey back down to stage 2, stage 3 and stage 4 sleep. This cycle repeats throughout the night, however, as the diagram below illustrates, we spend most of the first half of the night in deep sleep (slow wave or NREM), and most of the second half in REM sleep.
The last cycle is referred to as the ‘emergent cycle’ since it is during this one that we wake up. This last cycle contains no stage 3 or stage 4 sleep so under normal conditions we will emerge from either REM or stage 2 and the waking process may be accompanied by further hypnogogic images as was mentioned in stage 1. (Strictly speaking on waking these are referred to as hypnopompic).
The outline above describes a typical or average night’s sleep. Obviously there are large individual differences between people. Some may sleep much shorter periods, others who have been sleep deprived will spend longer in stage 4 and REM, and the pattern changes with age.
The Infradian Cycle
These occur over a period of time greater than 24 hours. In humans the best examples are menstrual cycle and PMS (Pre-Menstrual Syndrome) which occurs a few days prior to the onset of bleeding and is characterised (information for the boys), by loss of appetite, stress, irritability and poor concentration. There are a number of rhythms that are cyclic over about one year. A human example would be SAD (Seasonal Affective Disorder), more on this later; and in the animal world migration, mating patterns and hibernation of some species.
Seasonal Affective Disorder (SAD) (Infradian or circadian?)
Although it is apparently normal for most people to feel more cheerful in the summer months than in winter, a small number of people suffer an extreme form of this that appears to be related to the lack of bright light in the winter months.
As hopefully you’ll remember from the stuff we did on the physiology of sleep, light levels, as detected by receptors in the eye, influence levels of melatonin and serotonin. Additionally as you will hopefully recall from your work on depression, serotonin is implicated in mood. See how eventually all these strands knit together! At night low light levels stimulate the production of melatonin, this is what triggers sleepiness. Therefore you would expect the lower light levels of the winter months to have a similar affect.
In areas where light levels are exceptionally low for prolonged periods, such as the Polar regions, you would expect the effects to be particularly noticeable. Terman (1988) found that SAD was five times more common in New Hampshire, a northern state of the USA, than in Florida, obviously a sunnier clime.
Research evidence
The symptoms of SAD can be reduced in polar regions by sitting patients in front of very bright artificial lights for at least one hour per day. This lowers the levels of melatonin in the bloodstream which in turn reduces the feelings of depression. The precise mechanism for this is still unclear. It could be that melatonin (released from the pineal gland) has a direct affect on mood or it could have its influence indirectly through serotonin. Drugs used to treat depression such as Prozac and other MAOIs (monoamine oxidase inhibitors), appear to work by altering serotonin levels. Terman et al (1998) researched 124 participants with SAD. 85 were given 30 minute exposure to bright light, some in the morning, and some in the evening. Another 39 were exposed to negative ions (a placebo group).
Findings
60% of the am bright light group showed significant improvement compared to only 30% of those getting light in the evening. Only 5%of the placebo group showed improvement. The researchers conclude that bright light administered in this way may be acting as a zeitgeber and resetting the body clock in the morning.
Research into SAD has led to effective treatments suggesting that the theory has some validity. However, there does also appear to be a genetic component.
Note: SAD varies over a yearly cycle so can be viewed as an infradian (or circannual) cycle. However, it appears to disrupt the sleep/wake cycle so can also be viewed as circadian. SAD can be discussed in an essay on disruption of biological rhythms.
The menstrual cycle
Obviously a cycle that lasts about one month, so this cycle is infradian. Like other rhythms, the menstrual cycle appears to be under the influence of both internal (endogenous) mechanisms, and external zeitgebers.
Endogenous control
The cycle is under the internal control of hormones, particularly oestrogen and progesterone, secreted by the ovaries. These cause a number of physiological changes within the body including the release of at least one egg (ovum) from the ovaries and the thickening of the lining of the womb (uterus), in preparation for the arrival of the egg. If the egg is not fertilised then the lining of womb is shed and menstruation occurs. The contraceptive pill mimics the effects of pregnancy and cons the body into ceasing production of further eggs.
The outline above describes a typical or average night’s sleep. Obviously there are large individual differences between people. Some may sleep much shorter periods, others who have been sleep deprived will spend longer in stage 4 and REM, and the pattern changes with age.
The Infradian Cycle
These occur over a period of time greater than 24 hours. In humans the best examples are menstrual cycle and PMS (Pre-Menstrual Syndrome) which occurs a few days prior to the onset of bleeding and is characterised (information for the boys), by loss of appetite, stress, irritability and poor concentration. There are a number of rhythms that are cyclic over about one year. A human example would be SAD (Seasonal Affective Disorder), more on this later; and in the animal world migration, mating patterns and hibernation of some species.
Seasonal Affective Disorder (SAD) (Infradian or circadian?)
Although it is apparently normal for most people to feel more cheerful in the summer months than in winter, a small number of people suffer an extreme form of this that appears to be related to the lack of bright light in the winter months.
As hopefully you’ll remember from the stuff we did on the physiology of sleep, light levels, as detected by receptors in the eye, influence levels of melatonin and serotonin. Additionally as you will hopefully recall from your work on depression, serotonin is implicated in mood. See how eventually all these strands knit together! At night low light levels stimulate the production of melatonin, this is what triggers sleepiness. Therefore you would expect the lower light levels of the winter months to have a similar affect.
In areas where light levels are exceptionally low for prolonged periods, such as the Polar regions, you would expect the effects to be particularly noticeable. Terman (1988) found that SAD was five times more common in New Hampshire, a northern state of the USA, than in Florida, obviously a sunnier clime.
Research evidence
The symptoms of SAD can be reduced in polar regions by sitting patients in front of very bright artificial lights for at least one hour per day. This lowers the levels of melatonin in the bloodstream which in turn reduces the feelings of depression. The precise mechanism for this is still unclear. It could be that melatonin (released from the pineal gland) has a direct affect on mood or it could have its influence indirectly through serotonin. Drugs used to treat depression such as Prozac and other MAOIs (monoamine oxidase inhibitors), appear to work by altering serotonin levels. Terman et al (1998) researched 124 participants with SAD. 85 were given 30 minute exposure to bright light, some in the morning, and some in the evening. Another 39 were exposed to negative ions (a placebo group).
Findings
60% of the am bright light group showed significant improvement compared to only 30% of those getting light in the evening. Only 5%of the placebo group showed improvement. The researchers conclude that bright light administered in this way may be acting as a zeitgeber and resetting the body clock in the morning.
Research into SAD has led to effective treatments suggesting that the theory has some validity. However, there does also appear to be a genetic component.
Note: SAD varies over a yearly cycle so can be viewed as an infradian (or circannual) cycle. However, it appears to disrupt the sleep/wake cycle so can also be viewed as circadian. SAD can be discussed in an essay on disruption of biological rhythms.
The menstrual cycle
Obviously a cycle that lasts about one month, so this cycle is infradian. Like other rhythms, the menstrual cycle appears to be under the influence of both internal (endogenous) mechanisms, and external zeitgebers.
Endogenous control
The cycle is under the internal control of hormones, particularly oestrogen and progesterone, secreted by the ovaries. These cause a number of physiological changes within the body including the release of at least one egg (ovum) from the ovaries and the thickening of the lining of the womb (uterus), in preparation for the arrival of the egg. If the egg is not fertilised then the lining of womb is shed and menstruation occurs. The contraceptive pill mimics the effects of pregnancy and cons the body into ceasing production of further eggs.
For information
The menstrual cycle is divided into two phases--the follicular phase; and the luteal or ovulatory phase. The follicular phase includes the time when menstruation occurs and is followed by proliferation or the growth and thickening of the endometrium. This phase typically lasts from 10 to 14 days, starting with the first day of menstruation. Oestrogen and progesterone levels are at their lowest during menstruation. When bleeding stops, the follicular phase begins causing the endometrium to grow and thicken in preparation for pregnancy. During the next (approximately) two weeks, FSH levels rise causing maturation of several ovarian follicles and the size of the eggs triple.
FSH also signals the ovaries to begin producing estrogen which stimulates LH levels to surge at around day 14 of your cycle triggering one of the follicles to burst, and the largest egg is released into one of the fallopian tubes. This premenstrual period lasts approximately 14 days. After ovulation, LH causes the corpus leuteum to develop from the ruptured follicle. The corpus leuteum produces progesterone. Together estrogen and progesterone stimulate the endometrium to prepare a thick blanket of blood vessels that will support a fertilized egg should pregnancy occur. When pregnancy occurs, this blanket of blood vessels becomes the placenta which surrounds the fetus until birth.
External control (zeitgebers)
It has long been known that the menstrual cycle can be influenced by external factors, most notably by living with other women. The most likely mechanism for this is by the action of pheromones, chemical substances similar to hormones but which carry messages between individuals of the same species.
Armpit pheromones and the McClintock effect
The menstrual cycle is divided into two phases--the follicular phase; and the luteal or ovulatory phase. The follicular phase includes the time when menstruation occurs and is followed by proliferation or the growth and thickening of the endometrium. This phase typically lasts from 10 to 14 days, starting with the first day of menstruation. Oestrogen and progesterone levels are at their lowest during menstruation. When bleeding stops, the follicular phase begins causing the endometrium to grow and thicken in preparation for pregnancy. During the next (approximately) two weeks, FSH levels rise causing maturation of several ovarian follicles and the size of the eggs triple.
FSH also signals the ovaries to begin producing estrogen which stimulates LH levels to surge at around day 14 of your cycle triggering one of the follicles to burst, and the largest egg is released into one of the fallopian tubes. This premenstrual period lasts approximately 14 days. After ovulation, LH causes the corpus leuteum to develop from the ruptured follicle. The corpus leuteum produces progesterone. Together estrogen and progesterone stimulate the endometrium to prepare a thick blanket of blood vessels that will support a fertilized egg should pregnancy occur. When pregnancy occurs, this blanket of blood vessels becomes the placenta which surrounds the fetus until birth.
External control (zeitgebers)
It has long been known that the menstrual cycle can be influenced by external factors, most notably by living with other women. The most likely mechanism for this is by the action of pheromones, chemical substances similar to hormones but which carry messages between individuals of the same species.
Armpit pheromones and the McClintock effect
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Martha McClintock (1971) was the first to notice possible synchronisation of menstrual cycles amongst women living in close proximity whilst still an undergraduate student at Wellesley women’ liberal arts college in Massachusetts.
In 1988 McClintock & Stern published their findings of a 10 year longitudinal study into external control of the menstrual cycle. They had followed 29 women (aged 20-35) who had had a history of irregular menstrual cycles. Sweat samples from the armpits of 9 of the women had been collected, sterilised and dabbed onto the upper lip of the other twenty. Findings On 68% of occasions the recipients of the sweat donation had responded to the pheromones. Armpit compounds collected from the nine donors in the follicular phase of the menstrual cycle shortened the cycles of 20 recipients by 1.7 ± 0.9 days. Conversely, when the nine donors were in the ovulatory phase, the compounds lengthened the cycles of the same 20 recipients by 1.4 ± 0.5 days. |
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Evaluation
McClintock’s earlier work as well as the above study are supported by Russell et al (1980) who also placed dabs of sweat taken from the arm pits of sexually inactive women and placed on the upper lips of other women. Four out of five of the women had menstrual cycles that had synchronised to within one day of the sweat-donor.
However,
Due to the small sample size, the entire effect might have been due to just one or two subjects who had a disproportionate effect. Additional questions are raised by the following statement (Stern and McClintock, 1998): `Any condition preventing exposure to the compounds, such as nasal congestion anytime during the mid-cycle period from 3 days before to 2 days after the preovulatory, could weaken the effect. We analysed the data taking this into account'. It would be useful to know what a priori criteria were employed in making such adjustments, and whether the data analysis part of the project was done blind (Strassmann 1998). Wilson (1992) believes her results are due to statistical errors and that when these are corrected the effect disappears.
Wilson analyzed the research and data collection methods McClintock and others used in similar studies. He found significant errors in the researchers' mathematical calculations and data collection as well as an error in how the researchers defined synchrony. Wilson's own clinical research and his critical reviews of existing research demonstrated that menstrual synchrony in humans has yet to be proven. Wikipedia
Evolutionary advantages of external control of the menstrual cycle
Bentley (2000) believed that synchronisation between women living in close proximity would ensure that the women would conceive and give birth at similar times. This would be beneficial since they could share breast feeding, a behaviour observed in other species. Similarly, McClintock (1971) found that women who work in a mostly male environment have shorter menstrual cycles. In the past this would be of evolutionary advantage since it would provide more opportunities for pregnancy.
Some claim the opposite; synchronisation may be an evolutionary disadvantage. All the young in an area being born together would create an unhealthy competition for resources; food, nesting materials etc. Similarly, there would be too much competition for the fittest males (with the best genes). This would mean some females would have to settle for second best and reduce the fitness and adaptability of their own offspring. Evenly spread breeding seasons ensure the fittest males can be shared.
Light levels
Reinberg (1967) reported the case of a young woman who lived in a cave for three months with the only light being provided by a miner’s lamp. The woman’s daily cycle lengthened to 24.6 hours, (compare to Michael Siffre) and her menstrual cycle shortened to 25.7 days. It took a year before her cycle returned to normal! Reinberg believed that light levels could therefore influence the period of the cycle (no pun intended!). This theory is backed by research on 600 German girls that found that the onset of menstruation (menarche) is more likely in the winter months when light levels are low. The menarche also occurs earlier in girls that are blind. In Finland, during its very long summertime daylight hours, conception rates increase significantly. Perhaps you can think of other contributory factors! No football for example?*
Timonen et al (1964) found that women were far more likely to conceive in lighter months of the year than in darker months. This was attributed to the effects of light on the pituitary gland, which exerts its influence on the cycle via the ovaries.
However, much of the research has been carried out on non-human animal species so we have issues of generalisation. Breeding behaviour in humans is far more complex. The females of many species, including rats, simply need to be exposed to the right pheromone for them to adopt the lordotic stance (legs akimbo, bottom raised mating position). Clearly, outside of Essex at least, this is not the case with human females.
When humans participants have been involved they have tended to be case studies of individuals, and very often individuals with medical conditions, so again, generalisation is an issue.
Match of the Day
An interesting aside (and not to be quoted in essays). I’m a late Baby Boomer, born in a period of rapidly increasing population immediately after WWII. In the UK the Baby Boomer era ended in 1964. Coincidentally the same year that Match of the Day began. For the first time football was widely broadcast to the nation late every Saturday night. Rather than having an early night with the wife, men would have a few beers and watch the highlights of the day’s soccer. In those days, all games were played on a Saturday afternoon. The Baby Boomer years paid the penalty!
Endogenous Pacemakers and Exogenous Zeitgebers
Is the circadian rhythm determined by internal mechanisms or external factors?
As second year psychologists you should be able to guess the answer to this one. Whenever faced with an ‘is it nature or is it nurture’ question, it’s always BOTH!
First some terminology:
Endogenous: refers to internal, physiological factors
Exogenous: refers to external or environmental/social factors
Zeitgeber: we also have the added complication of this German word that roughly translated means ‘time giver’ and refers to exogenous factors that indicate times of day.
We shall consider the role played by endogenous and exogenous (zeitgebers) in the control of the circadian rhythm.
Endogenous
There is plenty of evidence to suggest that our biological rhythms are inherited. For example although within a species there is variation of rhythm, each individual tends to have a pattern of rhythm that shows little variation over a lifetime. Even the most extreme of environmental factors such as anaesthesia (not the late Russian Princess), alcohol and drug abuse, brain damage and loss of consciousness have little effect on our rhythms.
No surprises for guessing an area of the hypothalamus is responsible for endogenous control of the circadian rhythm in mammals. The supra-chiasmatic nucleus (SCN) is connected to the eyes via the optic nerve. It seems that the SCN contains a series of proteins that switch on and off very precisely and help maintain a constant internal rhythm. Light from the eyes, entrains or resets the internal clock, especially at certain times of the day. Exposure to blue light in the morning and darkness at night appear to be crucial times. Detection of darkness causes resetting at night, resulting in the secretion of melatonin, the sleep hormone, from the pineal gland.
Evidence for the role of the SCN
Mutant hamsters
Morgan (1995) removed the SCN from some hamsters and found that their rhythms ceased. However, when they received SCN transplants from other hamsters the cycles were re-established. In a follow up they transplanted the SCN from mutant hamsters (15 feet long!) who had shorter circadian rhythms. The hamsters receiving these SCNs developed these mutant cycles. (However, they did not grow to the same length!).
McClintock’s earlier work as well as the above study are supported by Russell et al (1980) who also placed dabs of sweat taken from the arm pits of sexually inactive women and placed on the upper lips of other women. Four out of five of the women had menstrual cycles that had synchronised to within one day of the sweat-donor.
However,
Due to the small sample size, the entire effect might have been due to just one or two subjects who had a disproportionate effect. Additional questions are raised by the following statement (Stern and McClintock, 1998): `Any condition preventing exposure to the compounds, such as nasal congestion anytime during the mid-cycle period from 3 days before to 2 days after the preovulatory, could weaken the effect. We analysed the data taking this into account'. It would be useful to know what a priori criteria were employed in making such adjustments, and whether the data analysis part of the project was done blind (Strassmann 1998). Wilson (1992) believes her results are due to statistical errors and that when these are corrected the effect disappears.
Wilson analyzed the research and data collection methods McClintock and others used in similar studies. He found significant errors in the researchers' mathematical calculations and data collection as well as an error in how the researchers defined synchrony. Wilson's own clinical research and his critical reviews of existing research demonstrated that menstrual synchrony in humans has yet to be proven. Wikipedia
Evolutionary advantages of external control of the menstrual cycle
Bentley (2000) believed that synchronisation between women living in close proximity would ensure that the women would conceive and give birth at similar times. This would be beneficial since they could share breast feeding, a behaviour observed in other species. Similarly, McClintock (1971) found that women who work in a mostly male environment have shorter menstrual cycles. In the past this would be of evolutionary advantage since it would provide more opportunities for pregnancy.
Some claim the opposite; synchronisation may be an evolutionary disadvantage. All the young in an area being born together would create an unhealthy competition for resources; food, nesting materials etc. Similarly, there would be too much competition for the fittest males (with the best genes). This would mean some females would have to settle for second best and reduce the fitness and adaptability of their own offspring. Evenly spread breeding seasons ensure the fittest males can be shared.
Light levels
Reinberg (1967) reported the case of a young woman who lived in a cave for three months with the only light being provided by a miner’s lamp. The woman’s daily cycle lengthened to 24.6 hours, (compare to Michael Siffre) and her menstrual cycle shortened to 25.7 days. It took a year before her cycle returned to normal! Reinberg believed that light levels could therefore influence the period of the cycle (no pun intended!). This theory is backed by research on 600 German girls that found that the onset of menstruation (menarche) is more likely in the winter months when light levels are low. The menarche also occurs earlier in girls that are blind. In Finland, during its very long summertime daylight hours, conception rates increase significantly. Perhaps you can think of other contributory factors! No football for example?*
Timonen et al (1964) found that women were far more likely to conceive in lighter months of the year than in darker months. This was attributed to the effects of light on the pituitary gland, which exerts its influence on the cycle via the ovaries.
However, much of the research has been carried out on non-human animal species so we have issues of generalisation. Breeding behaviour in humans is far more complex. The females of many species, including rats, simply need to be exposed to the right pheromone for them to adopt the lordotic stance (legs akimbo, bottom raised mating position). Clearly, outside of Essex at least, this is not the case with human females.
When humans participants have been involved they have tended to be case studies of individuals, and very often individuals with medical conditions, so again, generalisation is an issue.
Match of the Day
An interesting aside (and not to be quoted in essays). I’m a late Baby Boomer, born in a period of rapidly increasing population immediately after WWII. In the UK the Baby Boomer era ended in 1964. Coincidentally the same year that Match of the Day began. For the first time football was widely broadcast to the nation late every Saturday night. Rather than having an early night with the wife, men would have a few beers and watch the highlights of the day’s soccer. In those days, all games were played on a Saturday afternoon. The Baby Boomer years paid the penalty!
Endogenous Pacemakers and Exogenous Zeitgebers
Is the circadian rhythm determined by internal mechanisms or external factors?
As second year psychologists you should be able to guess the answer to this one. Whenever faced with an ‘is it nature or is it nurture’ question, it’s always BOTH!
First some terminology:
Endogenous: refers to internal, physiological factors
Exogenous: refers to external or environmental/social factors
Zeitgeber: we also have the added complication of this German word that roughly translated means ‘time giver’ and refers to exogenous factors that indicate times of day.
We shall consider the role played by endogenous and exogenous (zeitgebers) in the control of the circadian rhythm.
Endogenous
There is plenty of evidence to suggest that our biological rhythms are inherited. For example although within a species there is variation of rhythm, each individual tends to have a pattern of rhythm that shows little variation over a lifetime. Even the most extreme of environmental factors such as anaesthesia (not the late Russian Princess), alcohol and drug abuse, brain damage and loss of consciousness have little effect on our rhythms.
No surprises for guessing an area of the hypothalamus is responsible for endogenous control of the circadian rhythm in mammals. The supra-chiasmatic nucleus (SCN) is connected to the eyes via the optic nerve. It seems that the SCN contains a series of proteins that switch on and off very precisely and help maintain a constant internal rhythm. Light from the eyes, entrains or resets the internal clock, especially at certain times of the day. Exposure to blue light in the morning and darkness at night appear to be crucial times. Detection of darkness causes resetting at night, resulting in the secretion of melatonin, the sleep hormone, from the pineal gland.
Evidence for the role of the SCN
Mutant hamsters
Morgan (1995) removed the SCN from some hamsters and found that their rhythms ceased. However, when they received SCN transplants from other hamsters the cycles were re-established. In a follow up they transplanted the SCN from mutant hamsters (15 feet long!) who had shorter circadian rhythms. The hamsters receiving these SCNs developed these mutant cycles. (However, they did not grow to the same length!).
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The SCN may regulate other cycles. Rusak & Morin (1976) found that lesions to the SCN disrupted their breeding pattern (infradian rhythm). Instead of just producing testosterone during the mating season, the hamsters produced it all year round.
Mutant hamsters have been used as a green source of electrical energy in London. Using the London Eye as a giant wheel they can generate enough electricity to power Westminster and half of Kensington :) |
Mortal chipmunks
DeCoursey et al (2000) removed the SCNs from 30 chipmunks before returning them to the wild. One of the proposed functions of sleep is the idea that it keeps us quiet and restful at night when otherwise we would be prone to predation. The poor chipmunks returned to their burrows at night, nut having no sleep/wake cycle would remain restless and noisy. Predators therefore found them easy to find and trapped in their burrows many were consumed. Suggesting once again… no SCN, no biological rhythms!
Body clocks are everywhere
The SCN appears to be the location of the main clock but there are certainly others known as peripheral oscillators. Yamazaki et al (2000) found that tissues from the liver, lungs and other organs could maintain a constant 24 hour cycle despite being kept in vitro (outside the body).
Hall (1999) suggests these peripheral clocks may also be present in humans. The adrenal glands secrete a hormone cortisol each morning just before dawn, (‘the darkest hour’ according to Mama Cass!). Cortisol therefore must be controlled by a clock mechanism. Hall removed tissue from the gland and grew it in culture and found that it continued to secrete cortisol at the same time each day. Hall concludes that the tissue in our adrenal glands must possess an endogenous clock.
Damiola et al (2000) altered the feeding times of rats. They managed to alter the circadian rhythm of the liver by anything up to twelve hours to adapt to this new feeding regimen. However, their master clock (in the SCN) remained unaltered. This suggests that these peripheral oscillators can run independently of the circadian rhythm.
Animals
Clearly there are ethical and methodological issues here. Hamsters and rats have very different biorhythms to humans, both being largely nocturnal.
External Factors (zeitgebers)
As we saw with Siffre, the natural endogenous cycle appears to have a cycle of around 24.5 to 25 hours. External factors are therefore needed to entrain the rhythm daily and keep it to 24 hours. Light appears to be crucial in maintaining 24 hour cycles:
Campbell & Murphy (1998), in a bizarre experiment, shone bright lights onto the back of participants’ knees and were able to alter their circadian rhythms in line with the light exposure. The exact mechanism for this is unclear, but it seems possible that the blood chemistry was altered and this was detected by the SCN. It is worth mentioning that these findings have never been replicated!
Biological mechanisms (extension)
The above study suggests that light detection in the body may be more complex than we might believe. The fact that most blind people seem to be detecting light to reset their body clock also suggests cells other than rods and cones may be responsible.
The rods and cones both contain light sensitive opsin molecules. However, a mutant strain of mice that have retinal degeneration lose their rods and cones but retain their biological rhythms. Severing the optic nerve in mice however, does destroy the rhythm. This appears contradictory, unless we assume that there are receptors in the eye other than rods and cones!
There are a number of possible candidates. Initially Sancar and others suggested that cryptochromes (which detect blue light) might be passing on the information to the body clock. These are particularly interesting since they are also present in plants. Later research has implicated another chemical melanopsin. Eckler et al (2008) found that killing these cells in mice made entrainment impossible. The mice could not adapt to changing light conditions suggesting these cells are the detecting mechanism. This would explain Mile’s blind man study. Although the blind man has lost the ability to detect light using rods and cones (so is unable to consciously perceive light) other cells like those containing melanopsin are still detecting light at an unconscious level and passing on this information to the body clock.
Miles et al (1977) reported the case study of a blind man who had a daily rhythm of 24.9 hours. Other zeitgebers such as clocks, radio etc. failed to reset the endogenous clock and the man relied on stimulants and sedatives to maintain a 24 hour sleep/wake cycle.
However, the question remains, how do the majority of blind people still manage to maintain a 24 hour cycle?
Luce & Segal (1966), however, have shown that light levels can be over ridden. In the Arctic Circle people still maintain a reasonably constant sleep pattern, averaging 7 hours a night, despite 6 months of darkness in the winter months, followed by six months of light in the summer. This suggests that light may not be as important a factor as first thought. It’s effects can certainly be over-ridden.
In these conditions it appears to be social factors that act to reset endogenous rhythms rather than light levels.
Similarly with new-born human infants. There is little evidence of a circadian rhythm in the first few weeks but it has to be entrained by feeding and sleeping habits. The first signs appear by 6 weeks and by 6 months are fully entrained.
Conclusion
This is how I’d conclude my essay on biological rhythms, especially one answering the old favourite on internal and external control of rhythms.
Our biological rhythms therefore appear to be internally and externally controlled. Left to their own devices our internal clocks seem to be set to about a 25 hour cycle but external cues, especially light, resets our clocks daily. So why do we need internal and external control?
If control was entirely internal we would not be sensitive to external changes such as light levels. Species that hibernate or migrate would not adjust their behaviour. This could be fatal if winter came earlier than expected and animals had failed to prepare for winter in time or were still stuck in colder parts of the World.
If control was entirely external our rhythms would be too erratic and change day to day depending on weather conditions etc. We therefore have an internal mechanism that keeps us relatively stable but is sensitive to environmental factors that allow for adjustments based on weather conditions and available food.
DeCoursey et al (2000) removed the SCNs from 30 chipmunks before returning them to the wild. One of the proposed functions of sleep is the idea that it keeps us quiet and restful at night when otherwise we would be prone to predation. The poor chipmunks returned to their burrows at night, nut having no sleep/wake cycle would remain restless and noisy. Predators therefore found them easy to find and trapped in their burrows many were consumed. Suggesting once again… no SCN, no biological rhythms!
Body clocks are everywhere
The SCN appears to be the location of the main clock but there are certainly others known as peripheral oscillators. Yamazaki et al (2000) found that tissues from the liver, lungs and other organs could maintain a constant 24 hour cycle despite being kept in vitro (outside the body).
Hall (1999) suggests these peripheral clocks may also be present in humans. The adrenal glands secrete a hormone cortisol each morning just before dawn, (‘the darkest hour’ according to Mama Cass!). Cortisol therefore must be controlled by a clock mechanism. Hall removed tissue from the gland and grew it in culture and found that it continued to secrete cortisol at the same time each day. Hall concludes that the tissue in our adrenal glands must possess an endogenous clock.
Damiola et al (2000) altered the feeding times of rats. They managed to alter the circadian rhythm of the liver by anything up to twelve hours to adapt to this new feeding regimen. However, their master clock (in the SCN) remained unaltered. This suggests that these peripheral oscillators can run independently of the circadian rhythm.
Animals
Clearly there are ethical and methodological issues here. Hamsters and rats have very different biorhythms to humans, both being largely nocturnal.
External Factors (zeitgebers)
As we saw with Siffre, the natural endogenous cycle appears to have a cycle of around 24.5 to 25 hours. External factors are therefore needed to entrain the rhythm daily and keep it to 24 hours. Light appears to be crucial in maintaining 24 hour cycles:
Campbell & Murphy (1998), in a bizarre experiment, shone bright lights onto the back of participants’ knees and were able to alter their circadian rhythms in line with the light exposure. The exact mechanism for this is unclear, but it seems possible that the blood chemistry was altered and this was detected by the SCN. It is worth mentioning that these findings have never been replicated!
Biological mechanisms (extension)
The above study suggests that light detection in the body may be more complex than we might believe. The fact that most blind people seem to be detecting light to reset their body clock also suggests cells other than rods and cones may be responsible.
The rods and cones both contain light sensitive opsin molecules. However, a mutant strain of mice that have retinal degeneration lose their rods and cones but retain their biological rhythms. Severing the optic nerve in mice however, does destroy the rhythm. This appears contradictory, unless we assume that there are receptors in the eye other than rods and cones!
There are a number of possible candidates. Initially Sancar and others suggested that cryptochromes (which detect blue light) might be passing on the information to the body clock. These are particularly interesting since they are also present in plants. Later research has implicated another chemical melanopsin. Eckler et al (2008) found that killing these cells in mice made entrainment impossible. The mice could not adapt to changing light conditions suggesting these cells are the detecting mechanism. This would explain Mile’s blind man study. Although the blind man has lost the ability to detect light using rods and cones (so is unable to consciously perceive light) other cells like those containing melanopsin are still detecting light at an unconscious level and passing on this information to the body clock.
Miles et al (1977) reported the case study of a blind man who had a daily rhythm of 24.9 hours. Other zeitgebers such as clocks, radio etc. failed to reset the endogenous clock and the man relied on stimulants and sedatives to maintain a 24 hour sleep/wake cycle.
However, the question remains, how do the majority of blind people still manage to maintain a 24 hour cycle?
Luce & Segal (1966), however, have shown that light levels can be over ridden. In the Arctic Circle people still maintain a reasonably constant sleep pattern, averaging 7 hours a night, despite 6 months of darkness in the winter months, followed by six months of light in the summer. This suggests that light may not be as important a factor as first thought. It’s effects can certainly be over-ridden.
In these conditions it appears to be social factors that act to reset endogenous rhythms rather than light levels.
Similarly with new-born human infants. There is little evidence of a circadian rhythm in the first few weeks but it has to be entrained by feeding and sleeping habits. The first signs appear by 6 weeks and by 6 months are fully entrained.
Conclusion
This is how I’d conclude my essay on biological rhythms, especially one answering the old favourite on internal and external control of rhythms.
Our biological rhythms therefore appear to be internally and externally controlled. Left to their own devices our internal clocks seem to be set to about a 25 hour cycle but external cues, especially light, resets our clocks daily. So why do we need internal and external control?
If control was entirely internal we would not be sensitive to external changes such as light levels. Species that hibernate or migrate would not adjust their behaviour. This could be fatal if winter came earlier than expected and animals had failed to prepare for winter in time or were still stuck in colder parts of the World.
If control was entirely external our rhythms would be too erratic and change day to day depending on weather conditions etc. We therefore have an internal mechanism that keeps us relatively stable but is sensitive to environmental factors that allow for adjustments based on weather conditions and available food.
