Biopsychology Flashcards
(86 cards)
1
Q
What is the nervous system?
A
A specialised network of cells, it is the primary communication system which uses electrical and chemical signals.
2
Q
What is the nervous system divided into?
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Central nervous system (CNS) and the peripheral nervous system (PNS).
3
Q
What is the CNS?
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Brain and spinal cord.
4
Q
What is the PNS divided into?
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Somatic nervous system (SNS) and automatic nervous system (ANS).
5
Q
What is the ANS divided into?
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Sympathetic and parasympathetic.
6
Q
What is the somatic nervous system?
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System that controls conscious/voluntary activities. Made up of afferent and efferent neurons.
7
Q
What is an afferent neuron?
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Sensory neurons carrying sensory information.
8
Q
What is an efferent neuron?
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Motor neurons carrying instructions to effectors.
9
Q
What is the PNS made from?
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Nerves.
10
Q
What is the autonomic nervous system?
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Controls internal organs and glands (automatic responses).
11
Q
What is the parasympathetic branch of the ANS?
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Returns the body to routine, day to day activities (rest and digest).
12
Q
What is the sympathetic branch of the ANS?
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Stress related activities (fight or flight).
13
Q
What do the parasympathetic and sympathetic branches do when operating together?
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Maintain homeostasis.
14
Q
What is the endocrine system?
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Regulates all biological processes in the body, made up of glands and hormones, working alongside the nervous system.
15
Q
Explain the process of the fight or flight response.
A
Stressor is perceived.
Signal sent to hypothalamus which activates the sympathetic branch of ANS.
Adrenal medulla (part of adrenal gland) releases adrenaline into the bloodstream and releases noradrenaline.
Pupils dilate, increased breathing and heart rate, muscle tension, glucose released.
After stressor is gone, parasympathetic branch of ANS dampens response and returns the body to testing state.
16
Q
Name the types of neurons.
A
Sensory - carry messages from PNS to CNS, long dendrites, small axons.
Relay - connect sensory neurones to motor neurones, short dendrites, long axons.
Motor - connect CNS to effectors, short dendrites, long axons.
17
Q
Explain the process of firing a neuron.
A
When resting, the inside of the neuron is negatively charged compared to the outside.
When activated, the neuron becomes positively charged for a second.
This causes an action potential to occur.
And this created an electrical impulse.
18
Q
Explain chemical transmission between neurons.
A
Signals within a neurone are transmitted electrically, but between neurones is chemically. When the electrical impulse reaches the end of the neuron (presynaptic terminal), the release of a neurotransmitter is triggered from tiny sacs called presynaptic vesicles.
Bind to receptors or post synaptic neurone
Produce inhibitory or excitatory effects.
19
Q
What are neurotransmitters?
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Chemicals that diffuse across the synapse.
20
Q
Where do axons take the electrical signals?
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Towards the synapse.
21
Q
Where do dendrites take the electrical signal?
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Away from the synapse.
22
Q
What is excitation?
A
When a neurotransmitter increase the positive charge of a postsynaptic neuron.
This makes an increased likelihood that the post synaptic neuron will pass the electrical impulse.
23
Q
What is inhibition?
A
When a neurotransmitter increases the negative charge of a postsynaptic neuron.
This makes a decreased likelihood that the post synaptic neuron will pass on the electrical impulse.
24
Q
What is summation?
A
Whether the post synaptic neuron fires or not. The excitory and inhibitory influences are summed up.
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Ways of studying the brain
Post mortem - studying the brain after death, determine whether observed behaviour related to structural abnormalities.
Electroencephalogram (EEG) - measuring electrical activity in the brain, measuring wave patterns to help diagnose conditions.
Event-related potential (ERP) - isolating electrophysiological response of the brain to a specific sensory, motor or cognitive event, statistically analysing EEG data.
Functional magnetic resonance imaging (fMRI) - measure brain activity while a person is carrying out a task, detects radio waves from changing magnetic fields, detect which areas are rich in oxygen and therefore active.
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Strengths of post mortem
Allows more detailed examination of anatomical and neurochemical aspects (not possible with non-invasive scanning techniques).
Develop understanding of schizophrenia - Harrison (2000) due to post mortem examinations, researchers have been able to identify structural differences and evidence for neurotransmitters which are associated with the disorder
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Limitations of post mortem
Can lead to inaccurate findings - length of time between death and post mortem, drug treatments and age are all confounding influences. Findings might lack internal validity making it difficult to draw conclusions.
Retrospective - unable to follow up anything that arises from the examination, so conclusions drawn are often limited.
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Strengths of EEG
High temporal resolution - takes a reading from an active brain making it more accurate.
Useful for clinical diagnosis - epileptic seizures can be picked up on an EEG so it can help to diagnose brain abnormalities.
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Limitations of EEG
Can only detect activity in superficial regions of the brain, not deeper areas therefore information gained from EEGs is limited.
Poor spatial resolution (smallest feature that a scanner can detect) - cannot provide information on deeper regions of the brain so information is limited compared to fMRI.
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Strengths of ERPs
Good temporal resolution - takes readings every millisecond so there is an accurate measurement of activity.
Non-invasive - allows more patients to have an ERP which improves understanding of conditions.
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Limitations of ERPs
Poor spatial resolution - higher spatial resolution allows psychologists to discriminate between different brain regions with accuracy, unable to look at areas deeper in the brain.
Can only be interpreted by trained professionals, expensive, may minimise use of ERPs
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Strengths of fMRI
Non-invasive, no risk of physical harm
High spatial resolution (the smallest feature that a scanner can detect) - greater accuracy
objective - volume of blood can be measured showing fact rather than opinion.
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Limitations of fMRI
Poor temporal resolution (how quick it can detect changes) - unable to predict with a high degree of accuracy.
Small sample size in research - due to limited funding, difficult to generalise/low population validity.
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Localisation of function
Functions such as movement, speech and memory are performed in distinct regions of the brain.
The opposite view is that the brain acts holistically.
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Hemispheres of the brain
2 symmetrical halves - left and right.
Hemispheric lateralisation - functions are controlled by a particular hemisphere (language centres in left, visuospatial tasks best performed by right)
Each hemisphere of the brain controls the opposite side of the body - contralateral.
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Lobes of the brain
Cortex is subdivided into 4 lobes, each associated with different functions, damage to specific areas means that the functions associated with that area will also be affected.
Frontal lobe - motor area, brocas area
temporal lobe - auditory area, wernickes area
parietal lobe - somatosensory area
occipital lobe - visual area
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Frontal lobe
Motor area, controls voluntary movement.
Damage could cause loss of muscle function (fine movements or paralysis).
Effects are opposite side of the body to damage.
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Parietal lobe
Somatosensory area, detects sensations (touch, heat, pressure)
Damage could cause loss of sensation, neglect syndrome (reduces awareness of stimuli), agnosia (inability to identify objects and faces).
Effects are opposite side of the body to damage.
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Occipital lobe
Visual area, visual processing centre.
Damage could cause partial/complete blindness, cortical blindness (unable to see but to damage to structure of eye)
Effects are opposite side of the body to damage.
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Temporal lobe
Auditory area, receives and analyses speech bases information.
Damage could cause partial/complete hearing loss, cortical deafness (unable to hear but no damage to structure of the ear)
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Language centres of the brain
Language is restricted to the left.
Broca's area and Wernicke's area.
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Broca's area
Left frontal lobe, responsible for speech production.
Damage results in Broca's aphasia - patient understands but their own speech is slow and lacks fluency, difficulty with prepositions and conjunctions, demonstrated by Broca's famous patient Tan.
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Wernicke's area
Left temporal lobe, responsible for speech comprehension.
Damage results in Wernicke's aphasia - severe difficulty in understanding speech, no problems producing speech, speech they produce is fluent but meaningless and often contains neologisms (nonsense words).
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Case study for localisation of the brain
Phineas Gage - suffered severe brain damage but only his personality was affected, motor functions, vision, hearing and speaking skills still intact. If the holistic theory was correct, he would have suffered with many more issues.
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Evidence for localisation theory
Case studies - Tan (aphasia - Broca's area), Clive Wearing (amnesia - hippocampus), Phineas Gage (frontal lobe).
Strength - case studies suggest that these functions are localised in these areas. HOWEVER, these individuals experienced very specific brain damage, so it can be difficult to generalise to all cases of brain damage.
Brain scans - research, using fMRI, healthy participants show activation in Broca's area during a reading out loud tasks and Wernicke's area during listening task (Peterson et al 1988).
Strength - research is scientific and objective (unlike case studies), no bias when interpreting results - the results are what they are.
(A*) Neurosurgery - destroying or removing certain parts of the brain that are thought to contribute to psychological problems. For example, in OCD, cingulate gyrus appears to be more active. A bilateral cingulotomy to surgically interrupt the circuit, burn away the tissue using a gamma knife (radiation) or capsulotomy - probes into the top of the skull and heat the tips. Strength - Cosgrove and Rauch (2001) - cingulotomy was effective in 56% and capsulotomy in 67%. The surgery wouldn't work if the theory was not true and no other functions are damaged. HOWEVER, not all patients are helped.
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Evidence against localisation theory
Language localisation research - suggesting language systems are more distributed - 2016 review found that only 2% of modern researchers think that language is completely controlled by Broca's and Wernicke's area. 'Language streams' identified in the right hemisphere. This contradicts the localisation theory, findings suggest that the correct approach in arguing for localised vs holistic is dependant on the function that we are considering, it is too simplistic to say one or the other.
Lashley's rats research - trained rats to run a maze and then destroyed areas of their cortex (between 10% and 50%). It was found that it was the amount of brain destroyed not the specific part which led to worsening performance. Concluded that higher cognitive processes such as learning and memory are not localised, instead are distributed in a more holistically across the brain. There is an idea that the brain could compensate when damaged. HOWEVER, this research cannot be generalised to humans.
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Hemispheric lateralisation
Some physical and psychological functions are dominated by a particular hemisphere.
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Context for left and right brain
Right hemisphere can only produce rudimentary words and phrases, but it does not contribute emotional context. Suggestion that the left hemisphere is the analyser and the right hemisphere is the synthesiser, led people to the idea that there is 'left brain' people who are more scientific and 'right brain' people who are more creative.
HOWEVER, this idea is wrong, research suggests that people do not have a dominant side of their brain. Nielsen et al (2013) analysed brain scans from over 1000 people ages 7-29, no evidence for a positive side.
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Wiring in lateralisation
Many functions are not lateralised.
In the motor area, there is contralateral wiring - the right hemisphere controls movement on the left side of the body and vice versa.
Vision is both contralateral wiring and ipsilateral wiring (same side). Each eye has a left and right visual field, the left visual field of both eyes is connected to the right hemisphere and the right visual field is connected to the left hemisphere.
There is similar contralateral and ipsilateral wiring for auditory input
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Strength of theory of hemispheric lateralisation
Research evidence - Fink et al (1996), PET scans to identify which areas were active during a visual processing task.
One instruction - focus on fine details of a picture.
Findings - regions on left hemisphere were more active.
Second instruction - focus on whole photo.
Findings - regions of the right hemisphere were more active.
For visual processing, hemispheric lateralisation is a feature.
Research evidence to support the idea that lateralisation can change over time - Szaflarski et al (2006) found language became more lateralised to the left hemisphere with increasing age. HOWEVER, after the age of 25, lateralisation decreased with each decade of life.
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Limitation of the theory of hemispheric lateralisation
Idea of left and right brain people is wrong, research suggests that people do not have a dominant side of their brain. Nielsen et al (2013) analysed brain scans from over 1000 people ages 7-29, no evidence for a positive side.
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Split brain research (hemispheric lateralisation)
Corpus callosum connects the left and right hemispheres, a split brain operation severs this, usually done to reduce epilepsy.
Sperry (1968) studied 11 split brain patients and compared them to non-split brain patients.
1) picture/word shown to right visual field, info received by left hemisphere, participant could only describe what they had seen, this is because language is lateralised in the left hemisphere.
2) picture/word shown to left visual field, info received by right hemisphere, participants could not describe what they had seen, information received by the right hemisphere could not be controlled to the language centres in the left hemisphere.
3) picture/word shown to left visual field and asked to select a matching object, info received by right hemisphere, participants could not describe what they had seen but could select a matching object out of sight using their left hand, right hemisphere does have language comprehension but not speech or writing.
4) picture/word of an emotional object shown to left visual field, info received by right hemisphere, participant could not describe what they had seen but did have an emotional response, right hemisphere appears to experience its own emotional reactions.
Conclusion - certain functions are lateralised in the brain, this supports the view that the left hemisphere is verbal and the right hemisphere is emotional.
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Strengths of split brain research
Supporting research - Michael Gazzaniga (1989) - same findings as Sperry (could say words presented to right visual field, but not left), participants could draw (with left hand) the words presented to left visual field, shows that right hemisphere has language comprehension. This increases external reliability.
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Limitations of split brain research
Lack of control over variables as it was a quasi experiment (IV is naturally occurring), also split brain patients had severe epilepsy and the control group did not - this is a major cofounding variable because only one group had epilepsy, so it could be the condition explaining the split brain task results, not the actual split brain.
Oversimplified - the results are typical of right handed men
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Neural plasticity definition
Ability of the brain to change and adapt as a result of experience and new learning.
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What does neural plasticity do?
Plasticity increases the number of synaptic contacts from neuron to neuron, synapses help strengthen the connections between neurons. Number and strength of connections are linked to intelligence and other higher ability skills.
Plasticity is especially relevant during the early 'critical years', so during infancy, the brain experiences rapid growth in the number of synaptic connections. At birth, each neuron in cerebral cortex have 2500 synapses, by 3, number of synapses is 15000, 6x. (Gopnick et al (1999)).
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'Use it or loose it' (neural plasticity)
Very active synapses are likely to become stronger (long-term potentiation). If the neuron is stimulated repeatedly, a permeant neural change could potentially form, so we can physically consolidate a memory through repetition or exposure to experience.
Shown in research of taxi drivers, Maguire et al (2000) studied 16 London taxi drivers and found there was a high concentration of neurones (grey matter) in the posterior hippocampus and this was positively correlated with their time as a taxi driver. This area of the brain is involved in memory and spatial navigation, shows how the brain can permanently change in response to frequent exposure to a particular task.
Less active tend to become weaker (long-term depression).
As we mature connections that we do not use are deleted - neural pruning (Purcell and Zukerman (2011)).
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Limitations of neural plasticity (commentary point NOT evaluation).
Negative consequences - taking part in addictive behaviours, dopamine stimulates neurons in the dorsal striatum involved in forming habits can lead to tolerance and relapse in addicts. It can also cause changes in brain circuits which are important in deciding what we pay attention to.
Phantom limb syndrome, occurs in 80-100% of amputees and is often resistant to treatment. Thought to be due to cortical reorganisation of the somatosensory cortex, the brain remaps the part of the body's sensory circuit to another part of the body, so the information is referred elsewhere. Plasticity is not always a good thing.
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Strengths of neural plasticity
Objective supporting research - Mechelli et al (2004), learning a second language increases the density of grey matter in the left parietal cortex, more fluency = more density, learnt at a younger age = more density.
Bezzola et al (2012) 40 hours of golf training increased motor cortex activity in new golfers ages 40-60.
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Functional recovery definition
Example of neural plasticity that can occur after trauma. Healthy brain areas may take over functions of those areas that are damaged, destroyed or missing. It may form new synaptic connections close to the areas of damage which enables functioning to continue.
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Ways functional recovery can occur
Axonal sprouting - undamaged axons grow new nerve endings to reconnect neurons whose links were injured or severed. Undamaged axons can connect with other undamaged nerve cells, forming new neural pathways.
Denervation super sensitivity - undamaged axons that do a similar job to those that are damaged become aroused to a higher level to compensate for those that are lost, however this can have negative consequences such as being overstimulated to pain
Recruitment of homologous areas on the opposite side of the brain.
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Strengths of functional recovery research
Real world applications - this process can occur quickly, but after weeks/months it can slow down, then rehabilitation therapy may be required to further recovery. Example: constraint-induced movement therapy to help patients who have had strokes. They repeatedly practice using the affected part of their body whole the unaffected arm is restrained, research has shown that this significantly increases function. This is due to recruitment of homologous areas on the opposite side of the brain.
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Limitations of functional recovery.
Factors such as age and level of education may impact recovery rates - Elbert et al (1994), capacity for neural reorganisation is much greater in children than in adults. Schneider et al (2014) found that 40% of people who achieved a disability-free recovery had more than 16 years of education compared to about 10% of those who had less than 12 years of education.
Small samples of patients or case studies of individual patients - cannot generalise findings because sample does not cover the population or because circumstances are too unique. Case studies could also create results that are biased from the researcher.
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Infradian rhythms
Menstrual cycle, takes longer than 24 hours to complete.
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The menstrual cycle (infradian rhythms)
Monthly changes in hormone levels. A typical cycle lasts around 28 days.
An egg is released, uterus is prepared for implantation if fertilisation happens.
1) menstrual stage - menstruation starts on day 1, lasts around 4 days.
2) follicular stage - uterus forms thick spongy lining ready for fertilised egg (day 4-14)
3) ovulation phase - egg released from ovary into uterine tube (day 14 = peak fertility)
4) luteal stage) uterus lining maintained for 14 more days (until day 28).
Follicle stimulating hormone (FSH) - makes follicle mature in ovary. Only made in the first 1/2 of cycle, then inhibited.
Luteinising hormone (LH) - stimulates ovulation, inhibits FSH, causes follicle to develop into corpus luteum (produces oestrogen and progesterone), controls growth of uterus lining.
Levels of these hormones fluctuate during the cycle.
It is an endogenous system but it can be influenced by exogenous zeitgebers
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Endogenous system
Controlled by internal factors
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Exogenous zeitgebers
Factors external to the body
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How can exogenous zeitgebers influence the menstrual cycle
During their cycle, women will secrete pheromones. These are secreted outside the body by an individual and received by a second individual of the same species.
Stern and McClintock (1998), showed how menstrual cycles may synchronise due to the influence of pheromones. Studied 29 women with irregular periods, samples of pheromones were gathered from 9 participants at different stages of their menstrual cycle. Women were asked to place a cotton pad under their armpit for at least 8 hours on each day of their cycle, cotton pads were treated with alcohol and frozen. On day 1, the remaining 20 women had day 1 of cycle pads rubbed on their upper lip, also on day 2, etc. 68% of women experienced changes to their own menstrual cycle which brought them closer to the cycle of their 'odour donor'
Evolutionary advantage: if pregnancy is synchronised and the mother dies, there will be someone else who can feed the child (EEA)
It is also suggested that male pheromones may also be an exogenous factor that influence the menstrual cycle. McClintock (1971), reported that women who work with men have a much shorted menstrual cycle. Evolutionary advantage: women are mot fertile more often
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Seasonal affective disorder (infradian rhythms)
Type of infradian rhythm known as a circannual rhythm (repeating on a yearly cycle).
Also known as winter depression as symptoms are more apparent/severe in winter (persistent low mood, irritability, lethargic, loss of interest/pleasure in daily activities.
Evidence suggests that SAD is related to seasonal variations in the production of melatonin (mostly produced at night) which affects the production of serotonin which is implicated in depression.
Anti-depressants limit the reabsorption of serotonin so it increases.
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Limitations for synchronisation studies (infradian rhythms)
Extraneous and confounding variables - stress, diet, lifestyle, medication. Therefore findings are not always consistent, suggests that menstrual synchrony studies are flawed.
HOWEVER, some evidence of reliable findings, Russell et al (1980), applied pheromones (using cotton pad technique) to a group of sexually inactive women everyday for 5 months, there was also a control group. 4/5 in experimental group had menstrual cycles had synchronised.
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Strength of research into SAD (infradian rhythms)
Predictive validity - the theory can make accurate - predications about the occurrence of SAD. Terman (1988), nearly 10% of those living in New Hampshire (north) experienced SAD compared to only 2% in the southern state of Florida. Increases validity.
Real world applications - phototherapy. Strong light to reset the body's internal clock and is found to reduce the effects of SAD in about 80% of people. Regarded as a safer treatment. Improves peoples quality of life. Increases validity.
HOWEVER, some people report headache and eye strain. Rohan et al (2009) compared people with SAD who were treated with phototherapy to a group who received CBT. Found relapse rate of 46% in phototherapy group and 27% for the CBT group.
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Ultradian rhythms
Sleep cycle, takes less than 24 hours to complete.
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The sleep cycle (ultradian rhythms)
5 stages, based on 90 minute cycles. Each stage is characterised by a different level of brain wave activity. Can be studied with an EEG.
1) light sleep (most people would deny being asleep), body relaxes, hr and temp fall, hypnogogic state may occur (vivid perceptions eg.falling perceptions) Characterised by alpha waves (mid frequency, short amplitude)
2) light sleep which you can easily be woken, body relaxes, hr, bp and temp fall, characterised by alpha waves (high frequency, short amplitude) and sleep spindles (brain activity following muscle twitching lasting approx 25 seconds)
3+4) deep sleep, hr, bp and temp fall to their lowest point and growth hormones are secreted, sleep walking, talking and night terrors can occur, characterised by delta waves (low frequency, high amplitude) also known as slow wave sleep.
5) paradoxial sleep - deepest sleep, but brain waves resemble being awake, hr, bp increase, breathing becomes faster and more irregular, rapid eye movement (REM sleep), body is paralysed (stops you acting out your dreams), hardest stage to wake someone up from, theta waves (closely resemble activity in the awake brain)
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Strength of research into sleep cycle (ultradian rhythms)
Improved understanding of age-related changes in sleep - Obayan et al (2004), meta-analysis of 65 studies of sleep patterns across the lifespan, participants age 5-102. Found decrease in SWS (stage 3+4), 24% of total sleep at age 5 and 9% of total sleep at age 70. Sleep has less and less of a restorative function which may help explain various issues in older age. This can encourage people to make use of relaxation and medication as they get older.
Research carried out in sleep labs using EEGs - high temporal resolution, can help in clinical diagnosis.
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Limitations of research into sleep cycles (ultradian rhythms)
Significant variation between people - Tucker et al (2007), found large difference between participants in terms of the duration of each sleep stage, particularly stages 3+4, these differences could be biologically determined. This makes it difficult to describe a 'normal' sleep cycle in any meaningful way.
Research carried out in sleep labs, using EEGs - cannot detect activity in deeper areas of the brain, poor spatial resolution, artificial environment.
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Circadian rhythms
Sleep-wake cycle, occurs over a 24 hour period.
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Sleep-wake cycles (circadian rhythms)
Tend to go to bed and wake up at approximately the same time everyday.
Governed by endogenous pacemaker - biological 'clock' called SCN (suprachiasmatic nucleus) within the hypothalamus, takes in all information about the amount and quality of light taken in by the eye.
Light can reset the SCN, suggesting daylight is an important exogenous zeitgeber in the sleep-wake cycle.
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Michael Siffre (circadian rhythms)
Spent nearly 7 months living in a cave with no exogenous zeitgebers. His circadian rhythm sleep-wake cycle was allowed to 'free run'. At first it ranged from 25-32 hours, but eventually settled at 24.9 hours, not 24.
Similar results from Wever (1979), participants spend 4 weeks in a bunker, deprived of natural light, all but 1 participant settled into a 24.9 hour sleep-wake cycle.
Conclusions: our natural sleep-wake cycle is longer than 24 hours.
As his sleep-wake cycle was regularly 24.9 hours this is evidence of an endogenous pacemaker playing a role.
As we are in the real world we live to 24 hours suggesting that exogenous zeitgebers play a role.
Mustn't overestimate the influence that exogenous zeitgebers have on out internal biological clock. Folkard et al (1985) studied 12 people who lived in a dark cave for 3 weeks, given a clock which researchers sped up over the study, the day was 22 hours long, not 24. 11 of participants were unable to adjust to a 22 hour day showing that we have a strong internal biological clock that cannot be easily overridden by zeitgebers.
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Strength of research into circadian rhythms
Practical applications.
Medical treatment - in chronotherapeutics - how medical treatments can be administered in a way which corresponds to someone's biological treatments. Heart attacks are more likely in mornings, so taking medication last thing at night can reduce the risk of a heart attack (Bonten et al, 2015), increases effectiveness.
Shift work - desynchronisation, people working night shifts are more likely to have mental health issues and divorce. Most lorry accidents occur between 4 and 7 am, also shift workers are 3x more likely to develop heart disease. One suggestion is to rotate shifts with the clock, Czeisler et al (1982) tested this at a chemical plant in Utah and found that workers felt better and less tired, managers reported increased productivity and fewer errors. Real world health and economical productivity for shift workers.
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Limitations of research into sleep-wake cycle
Difficult to generalise - cave and bunker studies are based on very small samples. Other research suggests that sleep-wake cycles vary much more widely, Czeisler et al (1999) found individual differences in sleep-wake cycles varying from 13-65 hours. Duffy et al (2001) found some people are 'larks' and others are 'owls'. Difficult to discuss anything more than averages meaning the practical applications that had been developed from such research may not be as useful.
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Endogenous pacemakers
Internal body clock.
Sleep-wake cycle involves both SCN and pineal gland.
1) optic chiasm takes in information about the amount of light and quality taken in by the eye.
2) Information travels along the optic nerve and into SCN
3) SCN passes information to pineal gland
4) Pineal gland secretes melatonin in relation to the amount of light there is. Negative correlation, decrease in light = increase in melatonin.
5) Melatonin induces sleep, levels rise from dusk and reach a critical level, making us sleepy.
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Animal studies on SCN (endogenous pacemaker)
We can generalise these findings to humans because there is similar mechanisms in the brain.
DeCoursey et al (2000) chipmunk study - 30 chipmunks had their SCN connections destroyed, returned to their natural environment and observed for 80 days, sleep-wake cycle disappeared, after 80 days a significant number had been killed as they were awake when predators were hunting.
Ralph et al (1990) hamster study - mutant hamsters with 20 hour sleep-wake cycles were bred, SCN cells from foetal tissue of the mutant hamsters were transplanted into the brains of normal hamsters, they took on the 20 hour sleep-wake cycle because the SCN controls it.
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Strength of animal studies on endogenous pacemakers
Reliable findings - Morgan (1995) removed the SCN from hamsters and found that the sleep-wake cycle disappears, then transplanted SCN from mutant hamsters brede to have shorter cycles and found that the sleep-wake cycle returns but was shorter
. Stephan and Zucker (1972) damaged SCN in rats and found that the sleep-wake cycle was disrupted.
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Limitations of research into endogenous pacemakers
Too simplistic - focussed on the SCN in the brain, but may ignore other biological clocks we have in other parts of the body (lungs, pancreas and skin). Although they are influenced by the SCN they also act independently from it. Ignoring other complex influences on circadian rhythms.
When studying the role of endogenous pacemakers we cannot study them in isolation - Siffre attempted to remove as many exogenous zeitgebers as possible there were still some, such as artificial light and these could have reset the biological clock. Pacemakers and zeitgebers do interact, so attempting to isolate each factor reduces validity.
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Exogenous zeitgebers
Light is the key zeitgeber in sleep-wake cycle.
Campbell and Murphy (1998) showed that light can be detected by skin receptors, woke up 15 participants ay various times and shone a light pad onto the back of their knees, this changed their usual sleep-wake cycle by up to 3 hours.
Light as the key zeitgeber is also supported by case studies.
Miles et al (1977) documented circadian rhythms of man who was blind since birth, he had a strong 24.9 hour sleep-wake cycle, struggled to set his body to 24 hour cycle so much that he had to use sedatives to sleep. Strong evidence that light is key because it was the only exogenous zeitgeber that he lacked.
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Evidence against light as the key zeitgeber
People in the Arctic circle live in a world of endless days in the summer and endless nights in the winter, yet they are able to maintain a fairly regular sleep-wake cycle. Could suggest sleep-wake cycle is primarily controlled by endogenous pacemakers that can override environmental changes in light.
Or it could suggest that other exogenous zeitgebers have a part (social cues such as meal times). This can be seen in new born babies who are born with pretty random sleep-wake cycles surrounding parental schedules and mealtimes, circadian rhythms start to emerge at 6 weeks. This can also be seen in jetlag (internal body clock out of sync with external world), the most effective way to deal with this is to immediately adapt and ignore internal feelings.
