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Biopsychology Flashcards

1
Q

What are the key features and functions of the nervous system?

A

The nervous system is a specialized network of cells that serves as our primary communication system, using electrical and chemical signals.
FUNCTIONS:
To collect, process, and respond to environmental information.
To coordinate the workings of different organs and cells in the body.
In contrast, the endocrine system communicates through hormones.

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2
Q

What is the structure and function of the CNS?q

A

The brain and spinal cord form the central nervous system.
The brain is the center of conscious awareness.
The outer layer of the brain, the cerebral cortex, distinguishes higher mental functions from animals.
The brain has two hemispheres.
The spinal cord is an extension of the brain, responsible for reflex actions.
It passes messages to and from the brain and connects nerves to the PNS.

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3
Q

What is he structure and function of the PNS?

A

PNS transmits messages via millions of neurones to and form the nervous system
PNS divides into Autonomic and Somatic NS’s

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4
Q

What are the key features of the endocrine system?

A

works alongside nervous system to control vital functions in the body through the action of hormones
works more slowly than the nervous system but has widespread and powerful effects

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5
Q

What are glands?

A

organs in body that produce hormones
key glnd - pituitary gland controls release of hormones from other endocrine glands in body

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6
Q

What are hormones?

A

secreted in the blood stream
affect any cell in the body that has a receptor for that particular hormone

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7
Q

What does the sympathetic state do?

A
  • increases heart rate
  • increases breathing rate
  • dilates pupils
  • inhibits ddigestion
  • inhibits saliva production
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8
Q

What does parasympathetic state?

A
  • Decreases heart rate
  • Decreases breathing rate
  • Constricts pupils
  • Stimulates digestion
  • stimulates saliva production
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9
Q

What do the endocrine system and ANS do during a stressful event?

A
  • stressor percieved from hypothalamus activates the pitutitary
  • sympathetic nervous system is now aroused
  • Adrenaline released from medulla into bloodstream, causes fight/flight response
  • when threat passes, Parasympathetic NS takes over and reduces activities of the body that were increased by actions of the sympathetic branch
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10
Q

What is the structure and function of sensory neurones?

A

Carry messsages from PNS to CNS
long dendrites and short axons
located in PNS in clusters called ganglias

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11
Q

What is the structure and function of motor neurones?

A

connect CNS to effectors like muscles/glands
short dendrites and long axons
cell bodies may be in the CNS nut longer axond form part of PNS

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12
Q

Whar is the structure of the neurone?

A

cell body/soma - genetic material
dendrites - branch-like structures protrude from cell body. carry nerve impulses from neighbouring neurones towards cell body
axon - carries electrical impulses away from the cell body down the length of the neurone, protected by myelin sheath and nodes or ranvier speed uio transmission of the impulse

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13
Q

What is the structure and function of relay neurones?

A

connect sensory neurones to motor neurones. short dendrites and short axons

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14
Q

How does a neurone fire?

A

at resting state, inside is negatively-charged compared to the outside
when a neurone is activated, inside of cell becomes positively-charged for a split second causing
an action potential to occur
creates an electrical impulse that travels down axon towards the end of the neurone

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15
Q

What is a synapse?

A

gap between 2 neurones

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16
Q

What event occurs at the synapse?

A

when electrical impusle reaches end of neurone it triggers the release of neuroransmitter from tiny sacs called synaptic vesicles
once a neurotransmitter diffuses across the synapse, it is taken up by the postsynaptic receptor site on the next neuron so the impulse onl travels in 1 direction

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17
Q

What are neurotransmitters?

A

chemicals that diffuse across synapse to next neurone in chain

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18
Q

What neurotransmitters have an excitatory response?

A

Adrenaline -> increases positive charge of presynaptic neuron, increasing likelihood that post synaptic neuron will fire
Dopamine

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19
Q

What neurotransmitters have an inhibitory response?

A

Seretonin -> increasing negative charge of postsynaptic neurone, making it less likely the post synaptic neurone will fire
Dopamine

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20
Q

What is summation?

A

Excitatory and inhibitory influences are summed by the postsynaptic neuron.
To trigger an action potential, the total effect must reach a certain threshold.
If the overall effect of the neurotransmitter is inhibitory, the postsynaptic neuron is less likely to fire.
If the overall effect is excitatory, the postsynaptic neuron is more likely to fire.

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21
Q

What are 2 exmples of neurotransmitters?

A
  • Acetyl choline - found where motor neurone meets a muscle, causing muscles to contract
  • Seretonin - affects mood and social behaviour which is why it has been iimplicated as a cause of depression
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22
Q

What is localisation of function?

A

specific brain areas are responsible for specific functions

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23
Q

What hemisphere controls the right side of the body?

A

left

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24
Q

What is the cerebral cortex?

A

inner part of the brain
separates us from lower animals as it is highly developed

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25
Q

What are the 4 lobes of the cerebral cortex?

A

Motor Area
Somatosensory Area
Visual Area
Auditory area

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26
Q

What is the motor area?

A

controls voluntary movement
damages may result in loss of control over fine motor movements

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27
Q

Where is the motor area?

A

back of frontal lobe

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28
Q

What is the somatosensory area?

A

processes sensory information from the skin (touch, heat, pressure)

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29
Q

Where is the somatosensory area?

A

front of the parietal lobe

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30
Q

What is the visual area?

A

each eye sends information from right visual field to left visual cortex
and from left visual field to right visual cortex

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31
Q

Where is the visual area of the brain?

A

in occipital lobe at the back of the brain

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32
Q

What is the auditory area?

A

analyses speech based information
damage may produce partial hearing loss
more extensive damage, more serious the loss

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33
Q

Where is the auditory area?

A

in the temporal lobe

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34
Q

Where is Broca’s area?

A

left frontal lobe

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35
Q

What happens if there is damage to Broca’s area?

A

Broca’s aphasia:
slow speech, laborious, lacking in fluency

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36
Q

Where is Wernicke’s area?

A

left temporal lobe
produce language but have problems understanding it so produce fluent and meaningless speech
produce nonsense words as part of the content of their speech

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37
Q

What is Wernike’s area?

A

produce language but have problems understanding it so produce fluent and meaningless speech
produce nonsense words as part of the content of their speech

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38
Q

What are the evaluation points of Localisation of function in the brain?

A

+) brain scan evidence
C.P - > Lashley research
-) language localisation model is being questioned
+) Case study evidence

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39
Q

How is brain scan evidence a strength of LOF?

A

P - Brain scan evidence.
Ev - Petersen et al. (1988) found Wernicke’s area active during listening and Broca’s area during reading. Tulving et al. (1994) found semantic and episodic memories in different prefrontal cortex areas.
Ex - These studies provide scientific evidence for localisation of function.
L - Supports the validity of LOF, using reliable methods to make claims more credible.

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40
Q

How is research from Lashley a counter for brain scan evidence?

A

P - Contradictory research.
Ev - Lashley (1950) removed up to 50% of rats’ cortex and found no specific area was crucial for learning a maze.
Ex - Suggests higher cognitive processes are distributed holistically in the brain.
L - Challenges localisation theory, implying complex activities involve multiple brain areas working together.

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41
Q

How is the language localisation model being questioned a limitation?

A

P - The language localisation model is being questioned.
Ev - Dick and Tremblay (2016)
fMRI revealed involvement of the right hemisphere and thalamus.
Ex - Suggests language is organised holistically, not confined to specific areas.
L - Challenges the localisation model, showing brain functions rely on interconnected networks.

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42
Q

How is case study evidence a strength of localisation of function?

A

P - Case study evidence.
Ev - Phineas Gage’s brain injury led to a significant personality change.
Ex - However, generalizing from one individual is difficult, and interpretations may be subjective, reducing validity.
L - Highlights limitations of case studies in localisation research, as they may not provide reliable evidence for the wider population.

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43
Q

What are the evaluation points for hemispheric lateralisation and split brain research?

A

+) evidence of lateralised function in normal brains
+) support from more recent split-brain studies
-) causal relationships are hard to establish

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44
Q

How is evidence of lateralised function in normal brains a strength of hemispheric lateralisation?

A

P - Evidence of lateralised function in normal brains.
Ev - Fink et al. (1996) found PET scans show the right hemisphere activates for global elements, while the left hemisphere activates for finer details.
Ex - Suggests hemispheric lateralisation is normal, not limited to split-brain patients.
L - Strengthens hemispheric lateralisation by showing its role in everyday brain activity

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45
Q

How is support from more recent split-brain studies a strength?

A

P - Support from recent split-brain studies.
Ev - Luck et al. (1989) found split-brain participants were faster at identifying odd objects, suggesting the left hemisphere has superior processing abilities.
Ex - Supports Sperry’s findings on distinct hemisphere functions.
L - Strengthens the case for hemispheric lateralization, providing evidence for specialized roles of each hemisphere.

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46
Q

How are causal relationships being hard to establish a limitation of split brain research?

A

P - Hard to establish causal relationships.
Ev - Sperry’s research compared split-brain participants to controls, but the control group lacked epilepsy, a confounding variable.
Ex - Cognitive differences in split-brain participants may be due to epilepsy, not the procedure.
L - Limits causal conclusions about hemispheric lateralization, as epilepsy may have influenced the results.

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47
Q

What is hemispheric lateralisation?

A

Brain is divided into 2 hemispheres each with specialiswed functions

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48
Q

What is localisation?

A

Specific brain areas are responsible for specific functions

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49
Q

What is lateralisation?

A

certain functions are more dominant in 1 hemisphere

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50
Q

What is contalateral control?

A

RH controls left side of body

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51
Q

What are the language centres in the brain?

A

Broca’s area - frontal lobe, speech production
Wernikes area - temporal lobe - language comprehension

52
Q

What is split-brain research?

A

surgical separation of the brain’s hemispheres by cutting the corpus callosum, to treat severe epilepsy

53
Q

What was Sperry’s procedure?

A

Images or words were presented to only 1 hemisphere RVF for LH processing
Information presented to 1 hemisphere could not be shared with the other

54
Q

When was Sperry’s research?

A

1968

55
Q

What were the findings for the right visual field of Sperry’s procedure?

A

Objects shown to the RVF were processed
ppts can describe the object as language centres in LH

56
Q

What were the findings for the left visual field in Sperry’s research?

A

Ppts cannot name the object as there are no language centres in RH
can select matching object with left hand
can select related object

57
Q

What was the emotional response in RH in Sperry’s research?

A

when they saw a pinup picture shown to LVF, ppts giggled but reported seeing nothing

58
Q

What is brain plasticity?

A

the brain’s ability to reorganise itself by forming new neural connections throughout life.
Allows adaptation to new experiences or injuries

59
Q

What is synaptic pruning?

A

process where extra neurones and synaptic connections are eliminated to increase the efficiency of neuronal transmissions

60
Q

When does synaptic pruning happen?

A

throughout life but most prominent childhood and adolesence

61
Q

What was the Maguire et al (2000) study?

A

London Taxi drivers had increased grey matter volume in the posterior hippocamous compared to controls

62
Q

What is functional recovery after trauma?

A

healthy brain areas take over functions of areas damaged , destroyed or even missing
brain is able to rewire and reorganise itself by forming new synaptic connections close to the area of damage

63
Q

What is axonal sprouting?

A

growth of new nerve endings that connect with other undamaged neurones to form new neural pathways
aids in functional recovery after brain injury

64
Q

What is denervation supersensitivity?

A

when remaining neurones became more sensitive to neurotransmitters after nearby neurones are damaged

65
Q

What is recruitment of homologous areas?

A

process where the opposite hemisphere takes over functions of the damaged area

66
Q

What is spontaneous recovery?

A

rapid initial recovery of functions following brain injury without formal rehabilitation

67
Q

What is rehabilitation therapy?

A

Therapeutic interventions aimed at aiding recovery of function after brain injury

68
Q

What are the evalaution points for plasticity and functional recovery?

A

+) may not decline sharply with age
-) possible negative behaviourial consequences
+)RWA
-) neural plasticity may be related to cogntive reserve

69
Q

How is possible negative behaviourial consequences a limitation of plasticity?

A

P - Brain adaptation can have negative consequences.
Ev - Prolonged drug use reduces cognitive function and increases dementia risk. 60-80% of amputees experience phantom limb syndrome due to somatosensory cortex changes.
Ex - This shows brain adaptation can lead to issues.
L - Demonstrates neural plasticity’s dual nature, with both beneficial and maladaptive outcomes.

70
Q

How is plasticity not declining sharply with age a strength?

A

P - Plasticity does not decline sharply with age.
Ev - Bezzola et al. (2012) found that 40 hours of golf training increased motor cortex activity in participants aged 40-60.
Ex - This shows that neural plasticity continues throughout life.
L - Highlights the brain’s ability to adapt and recover in later life.

71
Q

How is real world applicaiton a strength of functional recovery?

A

P - Understanding plasticity has improved neurorehabilitation.
Ev - Constraint-induced movement therapy promotes recovery by practicing with the affected arm while restraining the unaffected one, encouraging axonal sprouting.
Ex - This shows how research helps medical professionals create effective interventions.
L - Highlights the value of plasticity in developing therapies for functional recovery.

72
Q

How is being related to cognitive reserve a limitation of neural plasticity?

A

P - Neural plasticity may relate to cognitive processes.
Ev - Schneider et al. (2014) found brain injury patients with more education had higher cognitive reserve and better chances of disability-free recovery.
Ex - 40% of patients with over 16 years of education achieved DFR, compared to 10% with less than 12 years.
L - Cognitive reserve is crucial in brain adaptation after trauma.

73
Q

What is fMRI?

A

Brain-scanning technique that measures changes in blood oxygenation and flow due to neural activity in specific areas

Determines which parts of the brain are involved in specific mental processes by detecting areas with increased blood flow

74
Q

What is EEG?

A
  • method that records electrical activity in the brain using electrodes placed on scalp
  • monitors overall brain activity nd detects abnormalities such as epilepsy, tumours, or sleep disorders
75
Q

What is ERP?

A

what is left when all extraenous brain activity from an EEG recording filtered out

type of brainwave triggered by partiular events

Studies congitive processes such as perception and attention by analyzing brain responses to specific stimuli

76
Q

What are post-mortem examinations?

A

analysing a persons brain after death to investigate structural abnormalities

identifies potential causes of neurological conditions experienced during life by comparing with a neurotypical brain

77
Q

What are the evaluation points for ways of studying the brain?

A

+) fMRI is risk-free and high spatial resolution
+) EEG has practical uses and high temporal resolution
-) causation and ethics post-mortem

78
Q

How is fMRI being risk-free and having high spatial resolution a strength of ways of studying the brain?

A

P - fMRI is risk-free and has high spatial resolution.
Ev - fMRI doesn’t use radiation, produces high-resolution images, and shows brain activity in detail down to the millimeter.
Ex - This allows fMRI to safely provide a clear picture of how brain activity is localised.
L - This strengthens fMRI’s reliability in studying brain function without health risks.

79
Q

How is EEG having practical uses and high temporal resolution a limitation?

A

P - EEG has practical uses and high temporal resolution.
Ev - EEG has helped understand sleep stages.
Ex - Its high temporal resolution measures brain activity within 1 millisecond.
L - Shows EEG’s real-world usefulness in studying fast brain processes and sleep patterns.

80
Q

How is causation and ethics a limitation of post-mortem’s?

A

P - Causation and ethics.
Ev - Brain damage observed in post-mortem studies may not directly link to cognitive deficits.
Ex - Ethical issues arise regarding consent after death in post-mortem studies.
L - These factors challenge the usefulness of post-mortem studies in psychological research due to causation concerns and ethical dilemmas.

81
Q

What are circadian rhythms?

A

periodic activity governed by:
internal biological clock(endogenous pacemakers)
external changes in environment (exogenous zeitgebers)
last roughly 24 hours
regulates processes like sleep,wake cycle

82
Q

What are ultradian rhythms?

A

periodic fluctuations that occur multiple times a day

83
Q

What are endogenous pacemakers?

A

internal biological clocks that regulate rhythms like SCN in hypothalamus

84
Q

What are exogenous zeitgebers?

A

external environmental cues
that influence biological rhythms by entraining them to a 24 hour cycle

85
Q

What did Siffre’s cave studies show?

A

in the absence of external cues like light, his free-running circadian rhytm settled to about 25 hours, suggesting endogenous pacemakers govern rhythms

86
Q

What did Aschoff and Wever’s study show?

A

ppts deprived of natural light displayed circadian rhythms of 24-25 hours reinforcing role of internal biological clocks

87
Q

What did Folkard conclude (1985)

A

When participants followed a manipulated 22-hour day, only one adjusted comfortably. This suggests endogenous pacemakers are stronger than exogenous zeitgebers.

88
Q

What is the role of the SCN in circadian rhythms?

A

The SCN receives light information from the optic chiasm and uses it to reset the internal clock, aligning the rhythm with external light-dark cycles.

89
Q

How does light function as a zeitgeber?

A

Light influences the SCN, helping to reset biological rhythms. This explains why we feel drowsy at night and alert during the day.

90
Q

What is a free-running rhythm?

A

A biological rhythm functioning without external cues (e.g., light). Research shows it typically lasts slightly longer than 24 hours (about 25 hours).

91
Q

What are infradian rhythms?

A

Biological rhythms with a cycle longer than 24 hours, such as the menstrual cycle and seasonal affective disorder (SAD).

92
Q

What regulates the menstrual cycle

A

The menstrual cycle is governed by rising and falling levels of estrogen (stimulates ovulation) and progesterone (prepares the uterus for pregnancy).

93
Q

What is the typical length of the menstrual cycle?

A

It is approximately 28 days, but can vary between individuals.

94
Q

What did Stern and McClintock (1998) investigate?

A

They studied whether pheromones could synchronize menstrual cycles through external cues.

95
Q

What were Stern and McClintock’s findings?

A

68% of participants experienced changes in their cycle that brought them closer to the cycle of their pheromone donor, suggesting synchronization through exogenous zeitgebers.

96
Q

What is seasonal affective disorder (SAD)?

A

A depressive disorder linked to reduced daylight during winter, disrupting infradian rhythms.

97
Q

How does melatonin affect SAD?

A

In winter, prolonged melatonin secretion (due to less light) reduces serotonin levels, contributing to depressive symptoms.

98
Q

What are ultradian rhythms?

A

Biological rhythms that occur more than once every 24 hours, such as the sleep cycle.

99
Q

What is the duration of one sleep cycle?

A

Approximately 90 minutes, cycling through five distinct stages.

100
Q

What happens during REM sleep?

A

REM sleep is the fifth stage of the sleep cycle. Brain activity resembles wakefulness, the body is paralysed, and dreaming occurs.

101
Q

What happens during Stages 1 and 2 of sleep?

A

Stage 1: Light sleep; characterized by alpha waves (high frequency, short amplitude). A person can be easily woken.
Stage 2: Alpha waves continue, with occasional sleep spindles (bursts of rapid brain activity).

102
Q

What happens during Stages 3 and 4 of sleep?

A

Known as deep sleep or slow-wave sleep (SWS).
Brain activity shifts to delta waves (low frequency, high amplitude).
It is difficult to wake someone in these stages, which are vital for restorative processes.

103
Q

What are the evaluation points of circadian rhytms?

A

+) medical treatment
-) shift work
C.P -> correlational research
-) generalisations are difficult to make

104
Q

How is application to medical treatment a strength of biological rhythms?

A

P: Research into circadian rhythms has real-world applications in medical treatments.
Ev: Circadian rhythms coordinate body processes, aiding chronotherapeutics—timing medications for maximum effect.
Ex: Aspirin reduces morning heart attack risk; Bonten et al. (2015) found it’s most effective when taken at night.
L: This highlights how circadian rhythm research improves drug treatment effectiveness.

105
Q

How is research being correlational a counter for shift work?

A

P: Circadian rhythm research is correlational, so desynchronization may not directly cause difficulties.
Ev: Solomon et al. found high divorce rates in shift workers could stem from missing family events.
Ex: For example, shift workers often miss milestones like birthdays or dinners, straining relationships.
L: This suggests adverse effects could stem from social, not biological, factors.

106
Q

How is shift work a limitation of circadian rhythm research?

A

P: Shift work disrupts biological rhythms. Boivin et al. (1996) found concentration dips at 6 am (circadian trough), increasing accidents.
Ev: Knutsson (2003) found shift workers are three times more likely to develop heart disease.
Ex: Research has economic implications for better managing shift work.
L: This shows the value of circadian research in improving health and safety.

107
Q

How is generalisations being difficult to make a limitation of circadian rhythms?

A

P: Generalizations are difficult in circadian rhythm research.
Ev: Studies like Aschoff and Wever’s or Siffre’s often use small groups or individuals.
Ex: Siffre’s internal clock slowed at 60, showing individual differences.
L: This limits the ability to make meaningful generalizations across a wider population.

108
Q

What are the evaluation points for biological rhythms?

A

+) research on menstrual cycle shows it’s evolutionary basis
-) methodology used in synchronisation studies

+) age-re;ated changes in sleep
-) individual differences in sleep stages

109
Q

How is the menstrual cycle having an evolutionary basis a strength of biological rhythms?

A

P - Menstrual cycle research highlights its evolutionary basis.
Ev - For ancestors, synchronized menstruation enabled simultaneous pregnancies.
Ex - In groups, orphaned babies could access breast milk, boosting survival rates.
L - This suggests synchronization is an adaptive strategy.

110
Q

How is the methodology used in synchronisation studies a limitaiton of biological rhythms?

A

P - One limitation is the methodology used in synchronisation studies.
Ev - Many factors can influence menstrual cycles, acting as confounding variables.
Ex - Apparent patterns may occur by chance, explaining why studies like Trevathan et al. (1993) failed to replicate Stern and McClintock’s findings.
L - This suggests menstrual synchrony studies are flawed.

111
Q

How is individual differences in sleep stages a limitation of biological rhythms?

A

P - One strength is individual differences in sleep stages.
Ev - Tucker et al. (2007) found large differences between participants in the duration of stages 3 and 4.
Ex - These differences are suggested to be biologically determined.
L - This makes it difficult to describe normal sleep in any meaningful way.H

112
Q

How is understanding age-related changes in sleep a strength of biological rhythms?

A

P - One strength is understanding age-related changes in sleep.
Ev - SWS reduces with age, and growth hormone produced during SWS becomes deficient in older people.
Ex - Van Cauter et al. (2000) suggest reduced sleep may explain impairments in old age; SWS can be improved with relaxation and medication.
L - This shows that knowledge of ultradian rhythms has practical value.

113
Q

What is a strength of endogenous pacemakers and exogenous zeitgeibers?

A

P - One limitation of SCN research is that it may obscure other body clocks.
Ev - Body clocks are found in many organs and cells and can act independently of the SCN.
Ex - Damiola et al. (2000) found that changing feeding patterns in mice altered liver cell rhythms for up to 12 hours without affecting the SCN.
L - This suggests there are many complex influences on the sleep/wake cycle beyond the master clock.

114
Q

What are the evaluation points for endogenous pacemakers and exogenous zeitgebers?

A

-) SCN research may obscure other body clocks
-) endogenous pacemakers cannot be studied in isolation
-) exogenous zeitgebers differ in different environment
-) case study evidence undermines effects of exogenous cues

115
Q

How is endogenous pacemakers not being studied in isolation a limitation of the endogenous pacemakers and exogenous zeitgebers?

A

P - Another limitation is that endogenous pacemakers cannot be studied in isolation.
Ev - Pacemakers are rarely free-running and are usually influenced by zeitgebers.
Ex - Studies like Siffre’s cave study are rare, and in real life, pacemakers and zeitgebers interact.
L - This suggests isolating pacemakers lowers the validity of the research.

116
Q

How is exogenous zeitgebers differing in environements a limitation of the endogenous pacemakers and exogenous zeitgebers?

A

P - One limitation is that the effect of exogenous zeitgebers differs in different environments.
Ev - People in areas with little darkness or light are affected differently.
Ex - The Inuit Indians maintain similar sleep patterns year-round, despite 6 months of darkness.
L - This suggests the sleep-wake cycle is mainly controlled by endogenous pacemakers, overriding environmental light changes.

117
Q

How is case study evidence undermining the effects if exogenous cues a limitation of he endogenous pacemakers and exogenous zeitgebers?

A

P - Another limitation is that case study evidence undermines the effects of exogenous cues.
Ev - Miles et al. (1977) reported a blind man with a 24.9-hour circadian rhythm.
Ex - Despite exposure to social cues like meal times, his sleep/wake cycle couldn’t be adjusted.
L - This suggests social cues alone aren’t effective in resetting the biological rhythm, and the natural body clock is stronger.

118
Q

What is the SCN?

A

primary endogenous pacemaker
tiny bundle of nerve cells in the hypothalamus which help maintain circadian rhythms

119
Q

How do nerve fibres from the eye contribute to the SCN’s reception of light information?

A

Nerve fibres from the eye cross at the optic chiasm on their way to the visual areas.
The SCN lies just above the optic chiasm and receives light information from this structure. This highlights the role of the optic chiasm in relaying light information to the SCN.

120
Q

What is melatonin?

A

hormone that induces sleep and is inhibited during periods of wakefulness
causal factor in seasonal affective disorder

121
Q

What is the pineal gland?

A

recieves information from SCN and increases production of melatonin at night

122
Q

What is entrainment?

A

resetting biological clocks

123
Q

What did research on DeCoursey et al (2000) tell us about the influence of SCN on sleep?

A

DeCoursey
destroyed SCN connections in he brains of 30 chipmunks which were returned to their natural hbitat and observed for 80 days.
Sleep/wake cycle disappeared and they were destroyed by predators

124
Q

What exogenous zeitgeber influences the sleep/wake cycle?

A

light - can reset body’s main endogenous pacemaker and also has an indirect influence on key processes in body controlling hormone secretion

125
Q

What did Campbell and Murphy 1988 do to show light was a key xogenous xeitgeber?

A

they woke 15 ppts at various times and shone a light on the back of their knees
produced deviation in sleep/wake cycle of 3 hours
light doesn’t rely on eyes to influence SCN

126
Q

How do social cues have an important influence on the sleep/ wake cycle?

A

sleep/wake cycle is random in newborns but most babies are entrianed by 16wks
parents imposing schedules is a key influence

127
Q
A

Psychology (12 decks)

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