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A-LEVEL PSYCHOLOGY > Biopsychology > Flashcards

Biopsychology Flashcards

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1
Q

What is the nervous system?

A

Specialised network of cells.
Primary internal communicatioin system
Two Main Functions:

  • Collect,process and respond to info and environment
  • Coordinate working of different organs and cells in the body

Divided into CNS and PNS

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2
Q

Draw and label the subdidivisions of the nervous system

A
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3
Q

What is the CNS?

A

Made up of brain and spinal cord

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4
Q

What is the brain as part of the CNS?

A
  • Centre of all concious awareness.
  • Cerebral cortex (outer layer) highly develpoed and is what distinguishes higher mental functions from animals.
  • Two hemispheres
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5
Q

What is the spinal cord as part of the CNS?

A
  • Extension of the brain.
  • Repsonsible for relflex actions
  • Passes messages to and from brain and connects nerves to PNS
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6
Q

What is the PNS?

A

Transmits messages via millions of neurones to and from CNS.

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7
Q

What is the PNS divided into?

A

Autonomic and Somatic Nervous System (ANS & SNS)

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8
Q

What is the ANS?

A
  • Involuntary system governs vital functions in body e.g. breathing, heart rate, digestion etc.
  • Controls smoth muscles and glands.
  • Control centre for this in brain stem
  • Contains only motor pathways
  • Subdivided into sympathetic and parasympathetic
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9
Q

What is the SNS?

A
  • Under concious control.
    • Controls muscle movement and recieves info from sensory receptors
  • Controls skeletal muscles and movement .
  • Control centres are in motor cortex.
  • Contains sensory and motor pathways.
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10
Q

What is the endocrine system?

A
  • Works alongside nervous system to control vital functions in body.
  • Slower
  • BUT very widespread and powerful effects
  • Various glands produce hormones
  • Hormones secreted into bloodstream.
    • Affect any cell in body that has receptor for particular hormone.
    • Most affect cells in several organs so leading to many diverse/powerful responses
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11
Q

What is the pituitary gland?

A
  • Produces growth hormones
  • In charge of system
    • Master gland - controls all glands in body
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12
Q

What is the adrenal gland?

A
  • Produces adrenaline
  • Fight or flight response
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13
Q

What is the thyroid gland?

A
  • Produces thyroxine.
  • Regulates how fast body digests (metabolism)
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14
Q

What is the fight or flight system?

A

Example of endocrine and autonomic system (ANS) working in parallel.

When stressor perceived (loud noise), ANS responds in an automatic way.

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15
Q

Describe the series of stages in the fight or flight response.

A
  • Hypothalmus triggers activity in sympathetic branch of ANS
  • ANS changes from resting parasympathetic to physiologically aroused sympathetic state.
  • Adrenaline released from adrenal medulla into bloodstream
  • Adrenaline triggers physiological changes im body (increased HR) creating physiological arousal necessary for response
  • Once threat has passes parasympathetic system returns body to resting state.
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16
Q

Describe the relationship of the parasympathetic and sympathetic branches of the ANS.

A
  • Parasympathetic in opposition to sympathetic (actions are antagonistic)
  • Acts as breaks and reduces activites of body that were increased by sympathetic branch
  • ‘rest and digest’ response
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17
Q

What is the sympathertic branch responsible for?

A
  • Increase HR
  • Increases breathing rate
  • Dilates pupils
  • Inhibits digestion
  • Inhibits saliva production
  • Contracts rectum
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18
Q

What is the parasympthetic branch responsible for?

A
  • Decrease HR
  • Decreases breathing rate
  • Constricts pupils
  • Stimulates digestion
  • Stimulates saliva production
  • Relaxes rectum
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19
Q

What are neurons?

A
  • Basic building blocks of nervous system - nerve cells that process and transmit messages through electrical and chemical impulses
  • 100 billion neurons (80%) in brain
  • Provide nervous system with its primary communication
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20
Q

Draw and label a typical neuron

A

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21
Q

What is the nucleus?

A
  • Control centre of cell.
  • Contains all chomosomal DNA
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22
Q

What is a dendrite?

A
  • Receives nerve impulse/signal from adjacent neurons
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23
Q

What is an axon?

A
  • Where the electrical signal passes along.
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24
Q

What is the myelin sheath?

A
  • Insulate/protects axon from external influences that might effect transmission of nerve impulse down the axon.
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25
Q

What are the Nodes of Ranvier?

A

Speed up transmission of impulse by forcing it to ‘jump’

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26
Q

What are the terminal buttons?

A
  • Send signals to an adjacent cell.
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27
Q

What is a sensory neuron?

A
  • Carry messages from PNS to CNS
  • Long dendrites
  • Short axons
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28
Q

Draw and label a sensory neuron

A
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29
Q

What is relay neuron?

A
  • Connect sensory neurons to motor or other relay neurons
  • Short dendrites
  • Short axons
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30
Q

Draw and label a relay neuron.

A
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31
Q

What is a motor neuron?

A
  • Connects CNS to effector like muscle/gland
  • Short dendrites
  • Long axons
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32
Q

Draw and label a motor neuron.

A
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33
Q

Describe electrical transmission

A
  • At rest, neuron negatively charged inside compared to outside
  • When activated by stimulus, inside becomes posivitely charged for split second causing action potential to occur.
  • Creates electrical impulse that travel down axon towards end of neuron.
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34
Q

Describe the basic reflex

A
  • E.g., knee-jerk
  • Stimulus (hammer hitting knee) detected by sense organs in PNS, conveying message along sensory neuron.
  • Message reaches CNS where it connects with relay neuron.
  • Then transfers message to motor neuron.
  • Then carries message to an effector (muscle) causing contraction and hence knee to move/jerk.
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35
Q

How do neurons communicate with other cells?

A

Synapses

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36
Q

What is a synapse?

A
  • Conjunction of a terminal button of one neuron and the membrane of another neuron, muscle cell/gland cell. Terminal button belongs to presynaptic neuron.
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37
Q

What is a presynaptic neuron?

A

Neuron that sends the message.

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38
Q

Describe signal within and between neurons.

A
  • Signals within neurons - transmitted electrically
  • Signals between neurons - transmitted chemically across a synapse
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39
Q

What is synaptic transmission?

A
  • Process where neighbouring neurons communicate by chemical messages across the synape that separates them.
  • Neuron receives messages from many terminal buttons and its terminal buttons form synpases with many other neurons.
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40
Q

Describe the processes involved in synaptic transmission.

A
  1. Electrical impulse (action potential) reaches presynaptic terminal
  2. Signal triggers release of neurotransmitter from synaptic vesicles
  3. Neurotransmitter diffuses across synpase.
  4. Neurotransmitters combine with receptors on postsynaptic membrane of adjacent neuron
    • specific molecular structure so fit perfectly into post-synaptic receptor site (e.g., lock and key)
  5. Stimulation of postsynaptic receptors by neurotransmitter result in excitation (depolarisation) or inhibition (hyperpolarisation) of -postsynaptic memebrane.
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41
Q

Draw and label a diagram for synaptic transmission

A
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42
Q

What is excitation?

A
  • Neurotransmitter (e.g adrenaline) increases positive charge of postsynaptic neuron.
  • Increases likelihood neuron will fire and pass on electrical impulse.
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43
Q

What is inhibition?

A
  • Neurotransmitter (serotonin) increases negative charge of post synaptic neuron.
  • Decreases likelihood neuron will fire and pass electrical impulse
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44
Q

Describe the excitatory and inhibitory influences.

A
  • Summed.
  • If net effect in post synaptic neuron is excitatory, neuron will be more likely to ‘fire’
  • If net effect is inhibitory the neuron wil be less likely to fire.
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45
Q

Are neurotransmitters excitatory or inhibitory?

A

Most can be both except GABA which is purely inhibitory.

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46
Q

Can an action potential travel in more than one direction? Why?

A
  • Only in one direction.
  • As synaptic vesicles containing neurotransmitter one present on and released from presynaptic membrane.
  • Also receptors for neurotransmitters only present on post synaptic membrane.
  • It’s binding of neurotransmitters to receptor which enables signal to be transmitted to next neuron.
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47
Q

Name the four ways to study the brain.

A
  • Functional Magnetic Resonance Imaging (fMRI)
  • Electroencephalogram (EEG)
  • Event-related potential (ERP)
  • Post-mortem examinations
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48
Q

What is fMRI?

A
  • Method used to measure brain activity while person performs task using MRI technology
    • detecting radio waves from changing magnetic fields
  • Enable reserachers to detect regions in brain rich in oxygen so active
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49
Q

How does fMRI work?

A

Detects changes im blood oxygenation and flow that occur due to neural activity in specific parts.

When brain more active consumes more oxygen and to meet increase demand bood flow directed to activated area (haemodynamic response)

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50
Q

What type of imaging does fMRI proudce and what does this show?

A
  • 3D imaging shows which parts of brain involves in particular mental process.
  • Has important implications for undertsanding localisation of function.
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51
Q

What is EEG?

A
  • Record of tiny electrical impulses produced by brain’s activity.
  • Measures characteristsic wave patterns which can help diagnose certain brain conditions.
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52
Q

How do EEGs work?

A
  • Via electrodes fixed onto sclap using skull cap.
  • Scan recording represents brain wave patterns that are generated from action of millions of neurons.
    • Provied overall account of brain activity
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53
Q

What are EEGs used for?

A
  • Often used by clinicians as diagnostic tool
    • unusual arrhythmic patterns of activity may indicate neurological abnormalities
    • (epilepsy, tumours/sleep disorders)
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54
Q

What are ERPs?

A

Brain’s electrophysiological response to specific sensory, cognitive/motor event can be isolated through statistical analysis of EEG data.

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55
Q

How are/do ERPs used/come about?

A
  • Statistical averaging technique - brain activity from original EEG filtered out leaving out responses to… specific task/stimulus
  • What remains - ERPs (types of brainwaves that triggered by particular events)
  • Research revealed that there are many forms of ERPs and how these are linked to cognitive processes (attention/perception).
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56
Q

What are post-mortem examinations?

A

Brain analysed after death to determine whether certain observed behaviours during parient’s lifetime can be linked to brain abnormalities.

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57
Q

When are post mortem examinations used and why?

A
  • Those with rare disorders/unusual deficits in mental processes/behaviour in lifetime
  • To establish likley cause of affliction person suffered. May also involve comparisons with neurotypical brain to ascertain extent of difference.
58
Q

Give 3 strengths of fMRIs

A
  • Non-inavsive (no harm)
  • More objective/reliable - useful to investigate psychological phenoma that people wouldn’t be able to provide in verbal reports
  • High spatial resolution - detailing by mm and clear picture of brain’s localisation.
59
Q

Give 2 limitations of fMRIs

A
  • Not direct measure of brain activity (measures changes in blood flow) - so not truly quantatative measure
  • Low temporal resolution - 5 second time lag behind image on screen and intial firing of neuronal activity
60
Q

Give 2 strengths of EEGs

A
  • High temporal reoslution can accuratey detect brain activity at resolution of single millisecond/less
  • Useful in clincal cdiagnosis (epilepsy) - disturbed brain activity so reading suddenly changes so help diagnose.
61
Q

Give two limitation of EEG

A

Only superfifcula areas not what’s happenig oni deeper regions (hypothalmus/hiippocampus)

Electrical activity picked up by several electrodes so not useful for pin pointing source (low spatial resolution)

62
Q

Give two strengths of ERPs

A
  • More specificity to EEG measurement of neural porcesses than use of raw data
  • Derived from EEG so high temporal resolution especially compared with fMRI so widespread use in meaurement of congitive functions and deficits.
63
Q

Give 4 limitations of ERPs

A
  • Lack of standardisation between different research studies which makes it diffcult to confirm findings
  • Signal small and difficult to pick out other electtrilca acitivity in brain so require many trial to gain meaningful data
  • Difficult to establish pure data as background and extraneous material must be eliminated and may not be easy to achieve
  • Strong voltage changes are recordable. Important electrical activities occurring deep in brain aren’t recorded
64
Q

Give two strengths of post mortem examinations

A
  • Allow more detailed exmaination of anatomical and neurochemical aspects of brain that wouldn’t possible using non-invasive. Examine deeper regions
  • Central part of understanding brain - Wernicke and Broca relied on this before neuroimaging was available.
65
Q

Give 4 limitations of PMEs

A
  • Causation - observed damage may not be linked to deficits but unrelated trauma/decay
  • Patients may not be able to provide informed consent. HM lost ability to form memories so couldn’t give consent yet post mortem conducted on his brain
  • Delay between death and study - confounding variables - drug treatments/ age of death
  • Retrospective as person already dead. Can’t follow up on anything that arises as possible relationship between brain abnormalities and cognitive functioning.
66
Q

Define localisation of function

A
  • Theory that different areas of the brain are responsible for different behaviours, processes or activities
67
Q

What was discovered in the 19th century and by who?

A
  • Paul Broca and Karl Wernicke found specific areas of brain associated with particular physical and psychological functions.
  • Before was thought all parts were involved in processing of thought and actions (holistic theory)
68
Q

What is the brain divided into?

A
  • Two symmetrical halves - right and left hemisphere
  • Some of physical and psychological functions are controlled/dominated by particular hemisphere (lateralisation)
69
Q

What are the hemispheres?

A

The left controls the right and the right controls the left.

70
Q

What is the outer layer of both hemispheres?

A
  • Cerebral cortex - covering that is about 3mm thick
  • Much more developed in humans than animals
  • Appears grey due to location of cell bodies (hence grey matter)
71
Q

Label the brain

A
72
Q

What is in the frontal lobe?

A

Motor area

73
Q

What is the motor area?

A

Controls voluntary movemetn in opposite side of body.

Damage may result in loss of control over fine movements.

74
Q

What is at the parietal lobe?

A

Somatosensory area

75
Q

What is the somatosensory area?

A
  • Processes sensory information such as touch from skin.
  • Amount of it devoted to particular body part denotes its sensitivity e.g. receptors for hands and faec occupy over half of the somatosensory area.
76
Q

What is in the occipital lobe?

A

Visual area

77
Q

What is the visual area?

A
  • Sends info from right visual field to left visual cortex and from left visual field to right visual cortex.
  • Damage to left hemisphere can produce blindness in part of right visual field of both eyes.
78
Q

What is in the temporal lobe?

A

Auditory Area.

79
Q

What is the auditory area?

A
  • Analyses speech-based information.
  • Damage may produce partial-hearing loss (more extensive damage more extensive loss)
  • Wernicke’s areas may particularly affect ability to comprehend language.
80
Q

Label THIS brain

A
81
Q

Which hemisphere is language restricted to in the brain?

A

Left hemisphere

82
Q

Outline Broca’s research

A

1880s - identified small area in left prefrontal lobe responsible for speech production.

83
Q

What does damage to Broca’s area cause?

A

Aphasia

84
Q

What is aphasia?

A
  • Characterised by speeach that is slow, labarious and lacking fluency
  • ‘Tan’ is all one his patients could say.
85
Q

Outline Wernicke’s research.

A
  • 1870s - No problem producing language but difficulty understanding it.
  • Speach was fluent but meaningless.
  • Left temporal lobe repsonsible for language comprehension so when damaged results in Wernicke’s aphasia.
86
Q

What is Wernicke’s aphasia?

A

Often produce nonsense words (neologisms) as part of content of speech.

87
Q

Give 3 strengths of localisation

  • Brain scan
  • Neurosurgical Evidence
  • Case Study
A
  • Peterson (88) - activity in Wernicke’s area (listening task) and Broca’s area (reading task). Suggests different areas have different frontals.
  • Dougherty (02) reported 44 OCD patients had a cingulatory (lesioning of cingulate gyrus). 32 weeks - 1/3 met criteria successful response and 14% partial repsonse to treatment. Suggests symptoms/ behaviours of serious mental disorder localised.
  • Phineas Gage damage from tampering iron removing chunk of frontal lobe. Quick-tempered, rude, ‘no-longer Gage’. Change in temperament suggests frontal lobe responsible for regulating mood.
88
Q

Give two limitations of localisation:

  • Existence of Cognitive Research
  • Not permanent as believed
A
  • Lashley (50) removed 10-50% of coretx in rats learning maze. No one area important than another in terms learning ability. Suggests higher cognitive functions (learning) not localised but distributed (holistic in brain).
  • When damaged & function compromised/lost, able to reorganise & recover function. Lashley - ‘law of equipotentially’ - same neurological action acheived. Not with all brain damage, but neural plasticity shows function of areas can be changed.
89
Q

What is plasticity?

A

Brain tendency to change and adapt (functionally and physically) as a result of experience and new learning.

90
Q

Describe infancy brain growth.

A

Growth in the synaptoc connections peaking at 15000 at age 2-3 years. Twice as many in adults.

91
Q

What happens to connections as we age?

A
  • Rarely used connections deleted and frequently used are strengthened (synaptic pruning)
92
Q

What can happen at any time to your neural connections?

A
  • Can change and new ones can be fromed as a result of learning and experience (plasticity)
93
Q

Who did research plasticity?

A

Eleanor Maguire et al. (2000)

94
Q

What was the procedure in the research into plasticity?

A
  • 16 right-handed male London taxi drivers participated (driving years >1.5 years)
  • Scans of 50 healthy males for comparison (didn’t drive taxis)
  • Mean age - same
  • MRI used to compare volume of hippocampus. - associated with development of spatial and navigational skills.
95
Q

What were the results in the research into plasticity?

A
  • MRI showed significantly more volume of grey matter in posterior hipposmapus in taxi driver (bigger)
  • Longer in job, more pronounced the structural differences were (+tive correlation)
96
Q

What were the conclusions in the research into plasticity?

A
  • Taxi drivers in london do test (‘The Knowledge’) assesing recall of possible routes.
    • Result of learning this seems to have altered the structure of their brains.
97
Q

What is functional recovery?

A
  • Form of plasiticity.
  • Following trauma damage, brain can redistribute/ transfer of functions usually performed by damage area(s) to other undamaged area(s).

Can occur quickly (spontaneous recovery) and the n slow after sevral weeks/months.

At this point individual may require rehabilitaition therparty to furtehr theri rehcovery.

98
Q

How fast can functional recovery happen?

A
  • Can occur quickly (spontaneous recovery) and then slow after several weeks/months.
  • At this point individual may require rehabilitaition therapy to further their recovery.
99
Q

What happens to the brain during recovery?

A

Rewires and reorganises by forming synaptic connections close to area damage.

Second neural pathways typically can’t carry out certain funtions but are activated/’unmasked’ to enabele functioning to continue.

100
Q

How is the process of brain recovery supported?

A
  • Structural changes
  • Axonal Sprouting - growth of nerve endings which connect other undamaged nerve cells to form neuronal pathways
  • Reformation of blood vessels
  • Recruitement of homologous are on opposite side of bain to perfom certain tasks e.g. damage Broca’s area on left could mean right side equivalent would carry out its function.
101
Q

Name 2 other pieces research into plasticity

A

Draganski et al. (2006)

Mechelli et al. (2004)

102
Q

Describe Draganski et al research.

A

Imaged brains of medical student 3 months before and after final exams

Learning induced changes in the posterior hippocampus and parietal cortex (presumabely as a result of exams).

103
Q

Describe Mechelli et al research

A

Found larger parietal cortex in brains of people who were bilingual compared to matched monolingual controls.

104
Q

Give some strengths and limitations of Maguire’s research

A
  • High control of variables - cause and effect - no extraneous varibles
  • Control group - increased hippocampus due to the ‘knowledge’
    • Factual dtad from MRIs. (empirical evidence - objective)
  • Samples sized differenr (16:50) - may not be large enough so could be chance.
    • Limited sample - only generalised to men
  • Random sample no mentioned
105
Q

Give two strengths of functional recovery and plasticity.

  • Practical application
  • Animal studies
A
  • Contributed to neurorehabilittaion. E.g. movement therapy/electrical stimulation to counter deficits to cognitive functional experienced s(troke). Brain may have capacity to fix itself requires further intervention to be successful.
  • Hubel Weisel (63) sewed one eye of kitten shut and analysed cortical responses. Area of visual cortex of shut eye not idle continued to process info from open eye. Shows neural plasticity does continue throughout lifespan.
106
Q

Give two limitations of functional recovery and plasticity.

  • Relationship between age and plasticity is complex
  • Individual differences
A
  • Reduces with age. Brain greater prospensity for reorganisation in childhood as constantly adapts. Bezzola (12) - 40 years golf training change neural representations of movement in participants 40-60. Contradiction - shows plasticity does continue throughout lifespan.
  • Evidence suggest educational attainment may influence how brain functionally adapts after injury. Schneider (14) more time injured patients spend in education (indication of cognitive reserve), greater chances of disability-free recovery,
107
Q

What is hemispheric lateralisation?

A
  • Idea two hemispheres functionally different and certain mental processes and behaviours mainly controlled by one hemisphere rather than the other.
  • In example of language (localised as well as lateralised).
  • Information received by one hemisphere to be sent to another through connecting bundles of nerve fibres (corpus callosum)
108
Q

What is split brain research?

A

Series of studying involves epileptic patients experienced surgical separation of hemispheres of brain to control seizures.

Known as commissurotomy - corpus callosum and other tissue connecting two heimpheres is cut to separate two hemispheres.

Allowed researchers to investigate extent brain function lateralised as two hemispheres in patients functioned independently and couldn’t share.

109
Q

Who did research into lateralisation?

A

Roger Sperry (1968)

110
Q

What was Sperry’s procedure?

A
  • Image/word projected to RVF (processed by LH) and same/different image couldn’t project to LVF (processed by RH)
  • Image flashed for 0.1 seconds so patient had no time to move eyes. ensures image/word remained in one visual field
  • ‘Normal’ brain corpus callosum would share info
  • Presenting image to one hemisphere of split-brain meant info couldn’t be passes between hemispheres.
111
Q

Describe the four of Sperry’s findings

A
  • Describing what you see
  • Recognition by touch
  • Composite words
  • Matching faces
112
Q

What were the findings for describing what you see?

A
  • Object shown to RVF - patients decribe what they see
  • Object shown to LVF - patients say nothing there
  • Can’t describe object in LVF because RH usually lacks language centres.
  • Messaged received by RH normally relayed via corpus collosum to language centre in LH.
113
Q

What were the findings for recognition by touch?

A
  • Object shown to LVF:
    • Couldn’t name could select matching object using left hand (connected to RH info from LVF)
    • Left hand could also select and object associated with image presented to LVF (e.g. ashtray selected when shown pictures of cigarette)
  • Couldn’t verbally identify what they’d seen (as LH needed for this) but ‘understand’ what object was (using RH) and select the corresponding object
114
Q

What were the findings for composite words?

A
  • Two words presented either side of visual field (key to left, ring to right)
  • Patient writes ‘key’ with their left hand (goes to RH linked to LVF)
  • Patient says word ‘ring’ (RVF linked to RH)
115
Q

What were the findings for matching faces?

A
  • Composite pictures of two different halves of a face was presented (one half to each hemisphere):
    • LH dominated verbal description
    • RH dominated the selection of a matching picture
116
Q

Give 3 evaluations for the theory of lateralisation.

  • Large amount of evidence
  • Changes with age
  • Differences may be overstated
A
  • Sperry & later Gazzaniga’s pioneering work produced impressive research findings. Main conclusion LH is more geared towards analytic/verbal tasks whilst RH more adept at performing spatial tasks, music, drawing and face recognition. LH is analyser whilst right is synthesiser.
  • Lateralisation of function appears not stay exactly same throughout lifetime, changes with normal ageing. Szaflarski (06) found language more laterlised to LH with increasing age of children and adolescents but after 25 decreased each decade of life. Possible use of extra processing resources of other Hs may compensate age-related declines in function.
  • Although verbal and non-verbal labels sometimes applied to summarise differences between Hs, modern neuroscientists say actual distinction less clear-cut/ messier. Normal brain - two Hs in constant communication and behaviour typically associated with one hemisphere be performed by other when required. Plasticity and functional recovery research demonstrates lateralisation is not always clear/permanent.
117
Q

Give 2 evaluations for split brain research

  • Strengths to methodology
  • Issues with generalising findings
A
  • Highly standardised procedured. Stare at ‘fixation point’ whilst eye blindfolded. Image flashed for 0.1s - no time ot move eye. Image wouldn’t spread across VFs. Allowed Sperry to vary aspects of basic procedure and ensured only one H receiving info at a time (high variable control)
  • Only 11 in all variations with history of epileptic seizures. May have caused unique changes in brain that may have influenced findings. Some also experienced more disconnection than others. Control was 11 with no history of epilepsy, may have been inappropriate. Limits extent findings generalised to normal brain, reducing validity of conclusions.
118
Q

What are biological rhythms?

A
  • What all living orhanisms are subject to.
  • They exert an important influence in the way body systems behave.
119
Q

What are the two things biological rhthyms are governed by?

A
  1. Endogenous Pacemakers
  2. Exogenous Zeitgebers
120
Q

What are endogenous pacemakers?

A
  • Body’s internal ‘clock’
121
Q

What are exogenous zeitbegers?

A

External changes in the environment.

122
Q

What are the three types of biological rhythms?

A

Ultradian rhythms

Circadian rhythms

Infradian rhythms

123
Q

What are ultradian rhythms? Give an example

A
  • Occur many times a day during the day
  • E.g., sleep-wake cycle - ultra diem meaning beyond a day
124
Q

What are circadian rhythms? Give an example.

A
  • Last for around 24 hours
  • E.g., sleep-wake cycle and core body temperature
125
Q

What are infradian rhythms? Give an example.

A
  • Longer than a day to complete
  • E.g., menstrual cycle - infra diem (below a day)
  • Circannual rhythms (about a year) - form of infradian rhythm taking much longer to complete e.g. hibernation/Seasonal Affective Disorder
126
Q

What is the sleep-wake cycle?

A
  • Refers to alternative states of lseep and waking
  • Dependent on 24 hours circadian cycle.
127
Q

How is the sleep-wake cycle affected by exogenous zeitgebers?

A
  • We feel drowsy when night time and alert during day.
  • Effect of daylight as an external signal for when we need to be awake.
128
Q

Describe further what endogenous zeitgebers are?

Include what SCN is.

A
  • Biological clock, left to its own devices, without external stimuli is called ‘free-running’.
  • Basic rhythm governed by suprachiasmatic nucleus (SCN).
  • Bundle of nerves within hypothalmus, lies just above optic chiasm and receives information about light directly from this structure.
129
Q

How is the sleep-wake cycle affected by endogenous zeitgebers?

A
  • Exogenous zeitgeber (light) can reset the SCN
  • SCN passes information on day length to the pineal gland which increases production of melatonin during night .
  • Melatonin is a hormone that induces sleep and inhibited during periods of wakefulness.
130
Q

What also happens to the cricadian rhythm during the slee-wake cycle?

A
  • Dips and rises in different times of the day.
  • Strongest sleep drive occurs in two ‘dips: 2-4am and 1-3PM (‘post-lunch dip)
  • Sleepiness we experienced during these circadian dips/troughs less intense if we’ve had sufficient sleep, and more intense when we are sleep deprived.
131
Q

Are sleep and wakefulness determined by the circadian rhythms alone? Why?

A
  • Also under homeostasis control.
  • When awake for long time, homeostasis tells us need for sleep is increasing due to amount of energy used up during wakefullness.
  • Homeostatic drive for sleep incereases throughout day, reaching its maximum in late evening when most people fall asleep.
132
Q

What other ‘clock’ is described as ‘free running’?

A
  • Internal circadian ‘clock’
  • Maintains cycle for about 24-25 hours even in absence of external cues.
  • However, system is intolerant of any major alterations in sleep and wake schedules (e.g. jet travel) as causes biological clock (and imternal physiological system dependent on this) to become completely out of balance.
133
Q

Who did reserach into circadian rhythms?

A

Michael Siffre (1960,1970)

134
Q

What did Siffre research?

A

Demonstrated a free-running circadian rhythms of about 25 hours

135
Q
A
136
Q

What research did Siffre do?

A
  • Spent long periods in dark caves to examine
  • Two months (61 days) in the cave of the Southern Alps (1962).
  • 6 months in Texan cave when 60 years (1970)
  • Had no external cues to guide rhythms- no daylight, clock or radio
  • Simply woke, ate and slept when he felt appropriate to do so (‘free-runnning’ circadian rhythm.
137
Q

What did Siffre find out?

A
  • In each case study his ‘free-running’ circadian rhythm settled down to just above usual 24 hours.
  • Had regular sleep/wake cycle
  • Later study found body clock ticked more slowly compared to when he was a young man, sometimes stretching his circadian rhythm.
138
Q

Who else did resreach into circadian rhythms?

A

Aschoff and Wever (1976)

139
Q

What was Aschoff and Wever research?

A

Group of partcicipants spent 4 weeks in WW2 bunker drpeoged of natural light

All but one (whose extened to 29 hours) displayed a circadian between 24 and 25 hours.

140
Q

Who did resreach into the influence of exogenous and endogenous zeitgebers?

A

Folkard et al (1985)

141
Q

What research did Folkard et al do?

A

Studied group of 12 people who live in dark cave for 3 weels, going to bed when the clock said 11.45 adn waking when it was 7.45

Researchers gradually speeded up clock (unbeknown to theparticipants0 so an apparent

A-LEVEL PSYCHOLOGY (22 decks)

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