BioPsych P2 Flashcards

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1
Q

Divisions of the nervous system

A

-Human nervous system splits into the central nervous system and the peripheral nervous system.

The central nervous system is made up of brain & spinal cord
the peripheral nervous system divides into the autonomic nervous system and the somatic nervous system.
The autonomic nervous system divides into the sympathetic and parasympathetic nervous system

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2
Q

Features of nervous system

A
  • Specialise network of cells
  • Primary communication system
  • Based on electrical and chemical signals.
  • Functions: 1 - to collect, process and respond to information in the environment, 2 - to co-ordinate the working of different organs and cells in the body
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3
Q

CNS

A

-Made of brain & spinal cord

Brain: Concsious awareness, outer layer ‘cerebral cortex’ is highly developed in humans - differentiates our higher mental functions from animals, divided into two hemispheres

Spinal Cord: extension of brain, reflex actions, passes messages towards/away from brain, connects nerves to Peripheral nervous system (PNS).

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4
Q

Peripheral Nervous system

A
  • Transmits messages via neurons to and from the nervous system.
  • Autonomic ns: governs vital body functions such as breathing, heart rate and stress responses. Divides further into sympathetic and parasympathetic ns.
  • Somatic ns: governs muscle movement and receives information from sensory receptors
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5
Q

Sympathetic Vs Parasympathetic

A

S: increases heart rate, breathing rate, dilates pupils, inhibits digestion, inhibits saliva production, contracts rectum. Responsible for Fight or Flight response.

PS: decreases heart rate, breathing rate, constricts pupils, stimulates digestion & saliva production, relaxes rectum. Responsible for Rest & Digest

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6
Q

Endocrine system

A
  • Works alongside nervous system to control vital functions through action of hormones.
  • More slow than nervous system - still has widespread & Powerful effects.
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7
Q

Glands

A

-organs which produce hormones
e.g. Pituitary gland aka ‘master gland’ controls the release of hormones form all other endocrine glands in the body.
Thyroid -> produces thyroxine, regulates body metabolism, brain development etc..
Pineal gland -> Produces Melatonin (sleep hormone)
Adrenal -> adrenaline

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8
Q

Hormones

A
  • Secreted into bloodstream
  • affect any cell in the body that has a receptor for a particular hormone

Ex. Thyrhoxine produced by thyroid affects cells in the heart and throughout body which increase metabolic rates -> increases growth rates.

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9
Q

Fight or Flight

A
  • Acute stress response
  • Shows endocrine and nervous system work together

SAM pathway:
Amygdala activates the hypothalamus -> activates sympathetic nervous system -> triggers adrenal medulla to release adrenaline & noradrenaline (neurotransmitter) -> facilitates the fight or flight response (increase in HR, breathing rate, dilate pupils)

HPA Axis: - chronic stress, longer lasting.
Activated by hypothalamus -> triggers pituitary gland -> release ACTH -> activates adrenal cortex which releases cortisol.

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10
Q

Sympathetic

A
  • increases heart rate
  • Increase breathing rate
  • Dilate pupils
  • Inhibits digestion
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11
Q

Parasympathetic

A
  • decrease heart rate
  • decreases breathing rate
  • constricts pupils
  • stimulates digestion
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12
Q

Neurons

A
  • 100 billion nerve cells in human nervous system, 80% located in the brain
  • Transmits signals electircally & chemicallly -> primary means of communication

3types of neurons; Sensory -> relay -> Motor

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13
Q

Sensory neurons

A
  • carry messages from the PNS to CNS
  • Long dendrites & Short axons
  • Located in PNS in clusters -‘ganglias’
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14
Q

Relay Neurons

A
  • connect sensory neurons to motor or other relay neurons
  • Short dendrites & short axons
  • 97% of neurons are relay & in the brain and visual system.
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15
Q

Motor Neurons

A
  • Connect the CNS to effectors such as muscles and glands
  • Short dendrites and long axons
  • Cell bodies are in CNS but long axons form part of PNS
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16
Q

Neuron structure

A
  • Cell body - nucleus → genetic material of cell
  • Dendrites → branch like, carry nerve impulses from neighbouring nerves towards cell body
  • Axon → carries electrical impulse away from cell body & down neuron: Covered in fatty layer → ‘myelin sheath’, gaps in axon → ‘nodes of ranvier’ speed up rate of transmission
  • Terminal buttons → communicate with the next neuron across synapse
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17
Q

Electrical transmission

A

a neuron is resting the cell is negatively charged

When neuron activates, cell becomes positively charged → action potential occurs

Creates an electrical impulse

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18
Q

A Synapse

A

each neuron separated from the next by a tiny gap → ‘synapse’

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19
Q

Chemical transmission

A

signals across a synapse are chemically transmitted

when the electrical impulse meets end of pre synaptic neuron, it triggers release of neurotransmitters from synaptic vesicles.

Once the neurotransmitter crosses the gap, it is taken up by a post synaptic receptor site on the neuron (can only travel one direction)

Chemical message is converted back into electrical impulse → electrical transmission begins

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20
Q

Neurotransmitters

A
  • chemicals which diffuse across the synapse to next neuron
  • each has it’s own molecular structure which is specific, fits perfectly with receptor site (lock &key)
  • Acetylcholine (ACH) found where a motor neuron meets a muscle, causes contraction
  • Serotonin - mood & social behaviour, implicated as a cause of depression
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21
Q

Excitation & Inhabitation

A

Neurotransmitters can have a excitatory or inhibitory affect on next neuron

  • Adrenaline - excitatory, increases positive charge, transmission will fire
  • Serotonin - inhibitory, increasing negative charge, transmission is less likely to fire
  • Dopamine - can be both
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22
Q

Summation

A

Excitatory and Inhibitory influences are summed up

  • must reach a certain threshold for action potential to be triggered in post synaptic neuron.
  • if net affect is inhibitory =less likely to fire
  • if net affect is excitatory =more likely to fire
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23
Q

Process of synaptic transmission

A
  1. Electrical impulse travels down the neuron to the terminal buttons
  2. The charge in the cell becomes positive → fires action potential down to terminal button
  3. Vesicle sacs bind with end of terminal button to release neurotransmitters
  4. Triggers Neurotransmitters to diffuse across synaptic cleft.
  5. NT reach next neuron and bind with the receptor sites
  6. Produce a excitatory or inhibitory affect through summation
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24
Q

Localisation of the brain - area info

A

Motor Area - in frontal lobe, responsible for voluntary movement, in both hemisphers

Somatosensory - Parietal lobe, receives sensory info, both hemispheres, L → RH R → LH

Visual Area - occipital lobe, receives and processes visual information, L → RH, R → LH

Auditory area - temporal lobe, analyses & processes acoustic info, LE → RH, RE →LH

Broca’s area - left frontal lobe, Speech production, damage → Broca’s aphasia ( slow speech, lacking in fluency)

Wernicke’s area - left temporal lobe, language comprehension, damage → produce fluent but meaningless speech .

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25
Q

Localisation of function (brain)

A

Specific areas of brain are linked with specific physical and psychological functions, if damaged the function of area is affected.

Lateralisation = some physical and psychological functions are controlled by a particular hemisphere.

Left side, left visual field etc is controlled by right hemisphere

opposite for right side of body

cerebral cortex covers the brain, is 3mm thick and highly developed (separates us from animals) ‘gray matter’

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26
Q

Limitation of Localisation of functions

A

Language localisation models has been questioned:

  1. Dick & Tremblay 2016, few researchers still believe language is only in broca’s and Wernicke’s area.

Advanced techniques e.g. FMRi have identified regions in the right hemisphere and the thalamus.

This suggests that language may be organised more holistically within the brain, contradicting this theory.

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27
Q

Strengths of Localisation - Support form neurosurgery

A

-Neurosurgery is used to treat mental disorders e.g. cingulatomy involves isolating the cingulate gyrus - disfunction may cause OCD.

Dougherty 2002, studied 44 ppl with OCD who had a cingulotomy. 30% met criteria for successful response & 14% for partial response.

The success of the procedure suggests that behaviours associated with mental disorders may be localised.

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28
Q

Strength of localisation - brain scan evidence

A

Petersen 1988, used brain scans to show activity in Wernicke’s area during a listening task and in Broca’s area during a reading task.

Tulving et al - Long term memory, revealed semantic and episodic memories are located in different parts of the prefrontal cortex.

→Many sophisticated & objective methods of measuring activity in the brain, providing good scientific evidence of localisation of function.

Lashley removed areas of cortex in rats learning the route through a maze. Learning required all of the cortex rather than a particular area. This suggests that higher cognitive processes aren’t localised but distributed in a more holistic way in the brain.

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29
Q

Hemispheric lateralisation

A

the brain is lateralised e.g. 2 hemispheres

some functions are localised, appear in both hemispheres.

RH produces rudimentary words but provides emotional context, LH is the analyser, RH = synthesiser

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30
Q

Contralateral

A

in motor area, the right hemisphere controls the left side of the body

the left hemisphere controls the right side of the body.

The left visual field for both eyes is connected to the RH, the right visual field for both eyes in connected to the LH. → enables visual areas to compare the different perspective from each eye & aids depth perception. same for auditory areas.

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31
Q

Hemispheric lateralisation limitation

A

the idea of the analyser vs the synthesiser brain may be wrong.

-there may be different function in the RH and LH but research suggests ppl don’t have a more dominant side, creating a different personality.

Nielsen 2013, analysed 1000 brain scans, finding ppl used certain hemispheres for certain tasks but no dominance.

→ this suggests that the notion of right or left brained people is wrong.

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32
Q

Hemispheric lateralisation evaluation strength

A

+ (evidence of lateralised brain functions in ‘normal brains’)PET scans show when normal ppt’s attend to global elements of an image, the RH is more active. When required to focus on finer details the specific areas of LH dominate (Fink 1996).

→ This suggests that hemispheric lateralisation is a feature of the normal brain as well as split brain

-

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33
Q

Split brain Procedure - Sperry 1968

A

split brain = 2 hemisphere’s surgically separated by cutting connections → corpus callosum

  • treat severe epilepsy → reduce electrical storm across hemispheres
  • 11 split brain ppt’s shown word/image to RVF and image shown to LVF - information couldn’t be conveyed across one hemisphere to another
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34
Q

Sperry 1968 findings

A
  1. Object show to RVF, ppt can describe what is seen as language centres are in LH
  2. Object shown to LVF: can’t name, can select matching object using left hand, can select objects associated with picture

pinup picture shown to LVF, ppt giggled but saw nothing

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35
Q

Sperry 1968 conclusions

A

-demonstrates how certain functions are lateralised in the brain, shows that LH is verbal and RH is ‘silent’ & emotional

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36
Q

Split brain eval strength - support from more recent research

A
  • Luck 1989, showed that split-brain ppt’s are better than normal controls e.g. Twice as fast at identifying the odd one out in array of similar objects
  • In the normal brain, LH superior processing abilities are reduced by the inferior RH.

This supports Sperry’s earlier findings that the ‘left brain’ and ‘right brain’ are distinct in terms of functions & abilities

37
Q

Split brain eval limitation - casual relationships are hard to establish

A
  • In S’s research, the behaviour of split brain ppt’s was compared to a neurotypical group.
  • none of control group has epilepsy, any differences may be due to the epilepsy not the split-brain.

This means that the unique features of the split-brain participants cognitive abilities might have been due to their epilepsy → therefore this study has low face validity

38
Q

Maguire 2000 taxi study

A
  • London taxi drivers had more grey matter in posterior hippocampus than control group
  • posterior hippocampus is used to develop spatial & navigational skills
  • used knowledge test
  • the longer they had been a london taxi driver, the grey matter was more profound
39
Q

Kuhn 2014

A
  • video games shown to give advantages which aren’t found in TV shows
  • ppt’s played super Mario for 30 mins per day over 2 months, compared to a control group, found significant differences in the grey matter in the cortex, hippocampus & cerebellum
40
Q

Draganski 2006 - supports maguire

A

took images of medical students brain 3 months before & 3 months after final exams

-found that learning induced changes were seen in the posterior hippocampus & parietal cortex as the result

41
Q

Davidson 2004 - meditation

A

study Tibetan monks & compared them to non-mediated controls

-each group meditated for a short period of time & were fitted with electrical sensors to detect brain activity

→ found the monk group showed significantly higher levels of gamma wave activity - helping to coordinate neuron activity

42
Q

Axonal pruning

A

synaptic connections are lost, due to lack of use

increases as we age

43
Q

Axonal bridging

A

synaptic connections are created due to use and new stimulus, during infancy there is a rapid growth of synaptic connections - peaks at 2-3 yrs at 15,000

44
Q

Brain plasticity

A

refers to how flexible our brain is depending on the stimulus we can change the function of our brain & it can adapt to new stimulu

45
Q

factors which affect brain plasticity

A

Learning a new skill

result of developmental changes

response to direct trauma to area of brain

response to indirect effects of damage e.g. swelling

46
Q

Plasticity & fr eval strength - gives psychologists deeper understanding of the brain

A
  • explains how as we learn our brain adapts to new stimuli to improve memory and how patients with brain trauma can recover & function as they did before the trauma.
  • Explains how functions of regions can adapt, Dragan ski….
  • as the hippocampus is responsible for long-term & short-term memory, it suggests that if the region is used for its function, it adapts by pruning and bridging → improving the regions ability to function.

→ therefor this helps psychologists understand the importance of the regions functions

47
Q

EVAL of BP and FR - limit, possible negative behavioural consequences.

A
  • the consewuences can cause pain 7 stress to the person after recovery
  • ex. 60-80% of amputees develop phantom limb syndrome as they experience sensations in the missing limb as if it were still there
  • Phantom limb syndrome can be painful and distressing but relieved by pain-relievers, antidepressants and narcotics the brain should stop sending signals to the missing limb.
  • this shows that the brain’s ability to adapt to damage is not always beneficial → leading to psychological & physical problems.
48
Q

Functional recovery - denervation super-sensitivity

A

-remaining axons become more sensitive

compensating for loss of axons in a pathway

causes pain

49
Q

functional recovery - constraint induced therapy

A
  • stopping patients from using coping strategies makes them improve using functional reorganisation
    e. g. Body Language
50
Q

functional recovery

A
  • healthy brain areas take over functions of areas damaged, destroyed or missing.
  • response occurs quickly after trauma & slows down - person may require rehabilitative therapy.

brain forms new synaptic connection close to area of damage, secondary neural pathways are activated to enable functioning to continue

51
Q

FR - recruitment of homologous areas

A

the opposite side of the brain takes over specific tasks e.g. language production.

52
Q

Functional magnetic resonance imaging

A
  • detects changes in blood oxygenation & flow that occurs to neural activity
  • if area is active, it consumes more oxygen and blood flow is directed to the active area
  • produce 3d images showing areas that are active
53
Q

FMRI Eval

A

+risk free and high spatial resolution, fmri doesn’t rely on radiation and is safe. Produces images with high spatial resolution showing high detail. TMT FRMI can provide a clear picture of how the brain activity is localised.

-expensive and poor temporal resolution, FMRI is expensive compared to other techniques, has poor temporal resolution due to the 5 second lag between neural activity and image. TMT fmri may not truly represent moment-to-moment brain activity.

54
Q

Electroencephalogram (EEG)

A
  • measures electrical activity within the brain using electrodes on a skull cap
  • records the brainwave patterns generated from thousands of neurons, showing overall brain activity.
55
Q

evaluation of EEG

A

+practical uses and high temporal resolution, eeg has contributed to understanding of stages of sleep, high temporal resolution shows brain acitivty in a millisecond. This shows the real-world usefullness

-information is generalised and source isn’t pinpointed. EEG produces generalised signal from thousands of neurons, difficult to know the source of neural activity. Therefore EEG’s can’t distinguish the activity of different but adjacent neurons.

56
Q

Event-related potentials (ERP)

A
  • measures brainwaves related to particular events
  • different forms of ERP and how these are linked to cognitive processes
57
Q

erp eval

A

+specificity and good temporal resolution, measures of neural processes more specific than EEGS, erps have excellent temporal resolution which is better than FMRI.

→ this means that ERP’s are frequently used in cognitive research

-lack of standardisation and background ‘noise’, makes it difficult to confirm findings in studies involving ERPs → background noise and extraneous material must be completely eliminated → these issues are a problem as they may not always be easy to achieve

58
Q

Post mortem

A

analysis of a dead person’s brain

areas are examined to establish the likely cause of a deficit or disorder that the person experienced in life.

may compare with a neurotypical brain to assess the extent of the difference

59
Q

post mortem eval

A

+localisation and medical research, Broca & Wernicke both relied on post-mortem studies, used to link HM’s memory deficits to damage in his brain

→ this means they continue to provide useful information

-knowing causations and ethics, observed damage in the brain may not be linked to deficits under review → PM raises ethical issues of consent after death. E.g. HM

→ this challenges their usefulness in psychological research

60
Q

circadian rhythms

A

one cycle every 24 hours

governed by endogenous pacemakers and exogenous zeitgebers

e.g. Sleep/wake cycle

61
Q

Sleep/wake cycle

A

governed by SCN (suprachiasmatic nucleus), lies above optic chiasm, provides information from eyes about light, light resets the SCN

  • exogenous zeitgebers = the affect of sunlight, we feel drowsy during night-time & alert during the day
  • endogenous pacemakers = a biological clock ‘left to it’s own devices’ w/o influence of external stimuli. ‘free-running’
    e. g. a 9pm melatonin secretion starts, 7:30am melatonin secretion stops, 10am highest alertness, 4;30 am lowest body temperature
62
Q

Siffre 1962

A

spent two months in a cave w/o natural light

  • thought is was mid-august when he came out when it was mid-september
  • his circadian cycle shifted to 25 hours although he had a normal sleep/wake cycle
63
Q

Aschoff & wever 1976

A
  • group of ppt’s spent 4 wks in a ww2 bunker w/o natural light.
  • all but one displayed a circadian rhythm between 24-25 hours

→ suggests that the natural sleep/wake cycle may be slightly longer than 24hrs but is entrained by exogenous zeitgebers associated w our 24hr day. e.g. daylight hours

64
Q

folkard 1985

A

studied a group of 12 ppl who lived in a dark cave for 3wks

they went to bed when clock said 11:45pm & woke up at 7:45 am.

The clock was speeded up to a 22 hour day

1/12 ppt’s adjusted comfortably, suggesting the existence of a strong free-running circadian rhythm not controlled by exogenous zeitegebers

65
Q

eval of circadian rhythms + strength, application to shift work

A

shift work creates desynchronization of biological rhythms, Bolvin 1996….

Research also suggests a link between shift work and poor health, w shift workers 3x more likely to develop heart disease

→ Therefore research into the sleep/wake cycle may have economic implications in terms of how best to manage shift work

66
Q

Bolvin 1996

A

found shift workers experience a lapse of concentration at 6am so accidents are more likely.

67
Q

Knutsson 2003

A

a link between shift work and poor health, w shift workers 3x more likely to develop heart disease

68
Q

circadian rhythms eval, strength - real world application to medical treatment

A

-circadian rhythms co-ordinate the body’s basic processes with implications for chronotherapeutics.

→ aspirin reduces heart attacks which are most likely to appear in the morning. Bonten 2015 found that taking aspirin is most effective the last thing at night

→ this shows that CR research can help increase the effectiveness of drug treatments

69
Q

circadian rhythms eval, strength - real world application to medical treatment

A

-circadian rhythms co-ordinate the body’s basic processes with implications for chronotherapeutics.

→ aspirin reduces heart attacks which are most likely to appear in the morning. Bonten 2015 found that taking aspirin is most effective the last thing at night

→ this shows that CR research can help increase the effectiveness of drug treatments

70
Q

CR eval limit - generalisations are difficult to make

A

studies of the sleep/wake cycle often use small groups of ppt’s or individuals.

→ ppt’s may not be representative of the wider population & this limits meaningful generalisations. Siffre observed that this internal clock ticked much more slowly at 60 than it did when he was younger.

→ this suggests that there are many factors which prevent general conclusions being drawn

71
Q

Infradian rhythms

A

less than one cycle in 24 hours

-female menstrual cycle, 28 days long. Rising oestrogen levels cause the ovary to release the egg, progesterone helps the womb lining thicken, readying womb for pregnancy, if not preggers = egg is absorbed & womb lining comes away

72
Q

Stern & McClintock 1998

A
  • studied 29 women with irregular periods
  • pheromones were taken from some at different stages of cycle, via a cotton pad in their armpits.

the pads were cleaned and rubbed against top lip of ppt’s.

68% of women experience changes to their cycle → closer to cycle of ‘odour donor’

73
Q

Seasonal affective disorder

A
  • Infradian rhythm
  • depressive disorder with a seasonal pattern
  • symptoms triggered during the winter months when number of daylight hours becomes shorter, ‘winter blues’
  • can be caused by melatonin, pineal gland secretes melatonin at 9pm until dawn when there is an increase in light

in winter this means that secretion goes on for longer & this has a effect on production of serotonin

74
Q

Infradian rhythms eval strength= its evolutionary basis

A

for our distant ancestors, it may have been advantageous for females to menstruate together & be pregnant at the same time.

→ in a social group, this would allow babies whose mothers died, to have access to breast milk, therefore increasing chances of survival

→ this suggests that synchronisation is an adaptive strategy

75
Q

Infradian rhythms eval limit = methodology used in synchronisation studies

A
  • there are many factors which change a womens menstural cycle & act as confounding variables
  • any supposed pattern may occur by chance this may be why other studies haven’t replicated Stern & McClintock’s original findings.

→ this suggests that menstrual synchrony studies are flawed

76
Q

Ultradian rhythms

A

occur more than once in 24hrs

-sleep cycle, sleep patterns occur in 90min periods, divided into 5 stages, each charachterised by a different level of brainwave activity

77
Q

sleep cycle

A

STAGE 1&2: light sleep - easily woke, S1 brainwaves are at a high frequency & short amplitude = alpha waves. S2 alpha waves continue

Stage 3&4: deep sleep/slow wave sleep, the waves have a lower frequency & higher amplitude, difficult to wake

Stage 5: REM sleep, Body is paralysed, brain produces theta waves & eyes move around, dreams occur

78
Q

evaluation of Ultradian rhythms + age-related changes in sleep

A

SWS reduces with age, growth hormone is produced during SWS so this becomes deficient in older people. → van Cauter 2000 suggested the reduced sleep may explain impairments in old age. Can be improved using relaxation and medication

→This suggests that knowledge of an ultradian rhythms has practical value

79
Q

eval Ultradian Rhythms - Limit, individual differences in sleep stages

A

-Tucker 2007, found large differences between ppt’s in the duration of stages 3 &4, they suggest that these differences are biologically determined.

→ this makes it difficult to describe ‘normal sleep’ in any meaningful way

80
Q

endogenous pacemaker & sleep/wake cycle

A
  • SCN is a primary endogenous pacemaker
  • scn is a tiny bundle of nerve cells in the hypothalamus → maintains CR

nerve fibres ffrom the eye cross at the optic chiasm towards the right & left visual areas. SCN lies above and recieve info about light

81
Q

DeCoursey 2000

A

destroyed SCN connections in the brains of 30 chipmunks which were returned back to their natural habitat & observed for 80 days.

-their sleep cycle disappeared & many were killed by predators

82
Q

Ralph 1990

A

bred ‘mutant’ hamsters with a 20hr sleep/wake cycle

SCN cells were transplanted from the foetal tissue of these hamsters into the brain of normal hamsters → developed 20hr cycles

83
Q

EPM Eval limit - obscure other body clocks

A

-Body clocks are found in many organs & cells. They are highly influenced by the actions of the SCN but can act independently.

Damiola 2000, showed how changing feeding patterns in mice altered CR of cells in the liver for up to 12 hrs, leaving the SCN unaffected.

→ this suggests that there may be many other complex influences on the sleep/wake cycle aside from the SCN.

84
Q

EPM eval limit - endogenous pacemakers can’t be studied in isolation

A

-only in exceptional circumstances ae endogenous pacemakers ‘free-running’ and unaffected by the influence of exogenous zeitgebers.

Total isolation studies are rare. In everyday life, pacemakers and zeitgebers interact so it makes little sense to separate the two.

→ this suggests the more researchers attempt to isolate the influence of internal pacemakers, the lower the validity of the research.

85
Q

exogenous zeitgebers & sleep/wake cycle

A
  • are external environmental factors that reset biological clocks - ‘entrainment’
  • w/o external cues, the free-running biological clock continues to ‘tick’ in a cyclical pattern. Zeitgebers reset the sleep/wake cycle

Light can reset the SCN.

86
Q

Campbell & Murphy 1998

A

Woke 15 ppt’s at various times & shone a light on the backs of their knees

producing a deviation in sleep/wake cycle of up to 3 hrs

87
Q

social cues

A

s/w c is random in newborns but most babies are entrained by 16 wks

schedules imposed by parents are the main influence e.g. Bedtimes

88
Q

EXZ eval limit - effects of EZ differ in different environments

A

-EZ don’t have the same effect on ppl who live in places where there is little darkness in summer and little light in winter. For example, the Innuit Indians of the artic circle have similar sleep patterns all-year round, despite spending six months in total darkness.

→ suggesting that the sleep/wake cycle is primarily controlled by endogenous pacemakers that ca override environmental changes in light.

89
Q

EXZ eval limit - case study evidence undermines effects of exogenous cues

A

-Miles 1977 reported the case of a man, blind from birth, with an abnormal CR of 24.9 hours.

Despite exposure to social cues like mealtimes, his s/w cycle couldn’t be adjusted.

→This suggests that social cues alone aren’t effective in resetting the biological rhythm & the natural body clock is stronger.