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Psychology A-level context + evaluation > Biopsychology > Flashcards

Biopsychology Flashcards

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1
Q

nervous system

A

two functions

  • collect, process and respond to info in environment
  • coordinate working of different organs and cells in the body.
  • divided into central and peripheral nervous system.
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2
Q

Central nervous system

A

brain and spinal cord that passes messages to and from the brain connected to the PNS

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3
Q

Peripheral nervous system

A

transmits messages via millions of neurons from CNS. Divided into autonomic NS and Somatic NS.

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4
Q

Autonomic nervous system

A

governs vital functions in body such as breathing, heart rate and digestion.

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5
Q

somatic nervous system

A

controls muscle movement and receives info from sensory receptors.

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6
Q

Endocrine system

A

controls vital functions in the body through action of hormones, alongside the nervous system.

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7
Q

Glands

A

produce hormones, major gland is the pituitary gland in the brain. It controls the release of hormones from all other endocrine glands.

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8
Q

Hormones

A

secreted through the bloodstream, effect any cell that has the particular receptor for the hormone. E.g. thyroxine produced by the thyroid affects cells in heart and any linked to metabolic rate.

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9
Q

Fight or flight

A

Stressor -> hypothalamus triggers sympathetic branch of ANS, arouses state.
Adrenaline released from adrenal medulla -> triggers physiological changes in organs e.g. quicker heart rate, dilated pupils, decreased saliva production.
threat passes -> parasympathetic nervous system returns body to resting state.

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10
Q

Three types of neurons

A

Motor neurons connect CNS to muscles and glands (short dendrites long axons)
Sensory neurons carry messages from PNS to CNS (long dendrites short axons)
Relay neurons connect sensory neurons to motor or other relay neurons (short dendrites and axons)

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11
Q

Structure of a neuron

A

Cell body - holds nucleus and genetic material
Dendrites - branches protrude cell body, carry nerve impulses.
Axon - carries electrical impulse away from cell body, covered in myelin sheath, gaps called nodes speed up impulses.
Terminal buttons - communicate with next neuron across synapse.

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12
Q

Firing of neuron

A

Resting state = negatively charged compared to outside

Activated = positively charged for a split second causing action potential to occur.

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13
Q

Synapse

A

gap between two neurons.

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14
Q

chemical transmission

A

Transmitted chemically. Electric impulse reach presynaptic terminal triggers the release of neurotransmitter from sacs called synaptic vesicles.Taken on by postsynaptic receptor and converted back into electric message.

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15
Q

Neurotransmitters

A

chemicals that diffuse across synapse. Each neurotransmitter has own specific molecular structure fits perfectly into postsynapse ( lock and key). E.g. acetylcholine (muscles contract) and Serotonin (affects mood and social behaviour).

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16
Q

Excitation and inhibition

A 
Adrenaline = excitatory, increases positive charge of postsynapse, more likely neuron will fire. 
Serotonin = inhibitory, increase negative charge, less likely neuron will fire. 
Dopamine = equally likely to be excitatory or inhibitory.
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17
Q

summation

A

Excitatory and inhibitory influences summed and reach a certain threshold for action potential to be triggered.

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18
Q

Holistic theory of localisation

A

scientists in 19th century - all parts of brain involved in processing, specific areas linked to specific physical and psychological functions. If parts are damaged, function is also affected.

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19
Q

Two hemispheres of the brain

A

Right hem = left side body

Left hem = ride side body

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20
Q

Cerebral cortex

A

like a ‘tea cosy’ covering inner parts of the brain. 3mm thick, separates us from lower animals. appears grey called ‘grey matter’.

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21
Q

Four lobes of the brain

A

Frontal
parietal
occipital
temporal

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22
Q

Areas inside the lobes.

A

Motor area = back of frontal lobe, controls voluntary movement.
Somatosensory area = front of parietal lobe, processes sensory info from skin.
Visual area = occipital lobe, eyes send info to both sides of brain, one side damaged could lead to blindness.
Auditory arear = temporal lobe, analyses speech based info, damage may produce hearing loss.

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23
Q

Broca’s area: speech production

A

left frontal lobe, damage causes broca’s aphasia (slow speech, difficulty finding words. Have difficulty with prepositions and conjunctions e.g. ‘a’, ‘the’

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24
Q

Wernicke’s area: language comprehension

A

back of temporal lobe, patients produce language but have difficulty understanding it. Wernicke’s aphasia causes nonsense words.

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25
Q

strengths of localisation theory

A
  • Brain scan evidence = Petersen used brain scans to show activity in broca’s and Wernicke’s area, suggesting different areas + Tulving LTM study = scientific evidence.
  • neurological evidence = removing or destroying parts of brain to control behaviour (freeman 50’s). Dougherty 44 OCD had cingulotomy 32 week follow up 1/3 met successful response.
  • support from case studies = Phineas Gage brain damage by accident, affected personality from calm to quick-tempered, frontal lobe may be responsible for regulating mood.
26
Q

Limitations of localisation

A
  • contradictory research = Lashley suggests higher cognitive functions, distributed in more holistic way. 10%-50% cortex removed in rats, no one area caused more or less difficulty in maze. involves whole brain.
  • neural plasticity is a challenge = brain recognises damage and uses other areas to chip in to the same action (Lashley), not all the time but stroke victims reported to recover fully.
27
Q

synaptic connections

A

once thought brain stopped growing in childhood, research now suggests connections can change and be formed at any time, due to learning and experience.

28
Q

studies of plasticity - Maguire

A

more volume of grey matter in posterior hippocampus in London taxi cab drivers to control group, linked to development of spatial and navigational skills. Had to take tests on locations - longer the job bigger the grey matter.

29
Q

studies of plasticity - Draganski

A

imaged brains of medical students 3 months before and after final exams, changes seen in posterior hippocampus and parietal cortex.

30
Q

recovery after trauma

A

healthy brain takes over functions of damaged brain. Process occurs quickly after trauma and then slows down - patient may then need rehabilitative therapy.

31
Q

new synaptic connections in recovery

A

brain able to rewrite functions forming new synaptic connections close to area of damage. activated as ‘unmasked’ to enable functioning to continue.

32
Q

Structural changes in recovery

A
  • Axonal sprouting = growth of new nerve endings connect undamaged cells to new neuropathways.
  • reformation of blood vessels
  • Recruitment of homologous areas = use other side of brain to perform specific tasks.
33
Q

Strengths of plasticity

A
  • practical application = contribution to neurorehabilitation e.g. movement therapy + electric stimulation to counter cognitive deficits after stroke. Requires further intervention.
  • Animal studies = kitten study, one eye sewn shut to see cortical responses (hubel and wiesel) info continued through open eye. loss of function leads to compensatory activity.
34
Q

Limitations of plasticity

A
  • potential negative consequences - maladaptive behavioural consequences e.g. prolonged drug use lead to poor cognitive functioning. 60-80% amputees suffer Phantom limb syndrome - continuing sensations of limb.
  • age and plasticity - reduces with age. Better reorganisation skills in childhood always adapting. Bezzola = 40 years of golf training produced changes in P’s aged 40-60. Plasticity does continue.
  • Related to cognitive reserve - Schneider found the more time brain injury patients spent in education the greater the chance of disability-free recovery. cognitive reserve crucial in recovery
35
Q

Hemispheric lateralisation

A

concerns behaviours controlled by just one hemisphere, e.g. language controlled by left hemisphere

36
Q

split-brain studies

A

Sperry - brain connected by corpus callosum sometimes cut to stop epilepsy. Studied patients who had the operation.

37
Q

Sperry’s study

A

image or word projected to a patients RVF and another to LVF. Corpus callosum shares info.
Object shown:
RVF -> patient easily describes what is seen.
LVF -> nothing there. could be recognised by touch, couldn’t verbally understand it.

38
Q

sperry’s words and matching faces

A

LH - dominated the verbal description

RH -dominated selection of a matching picture

39
Q

Strengths of split brain

A
  • Research lateralised brain functions = LH analytical and verbal, RH spatial tasks and music. However distinction may be too simplified and several tasks associated with one hemisphere.
  • Sperry’s methodology = Used standardised procedure presenting visual info to one hemisphere. flashed for 0.1 seconds so P’s had no time to move eyes and spread info. Controlled procedure.
  • debate of nature of brain = triggered philosophical debate, nature of consciousness + communication of hemispheres. Pucetti duality of brain, others argue hemispheres highly integrated, working together. Complex debate.
40
Q

Limitations of split- brain research

A
  • generalisation of sperry’s work = findings not widely accepted, split brain is unusual sample. Only 11 P’s, epilepsy caused unique changes in the brain. cant be generalised to normal brains lacking validity.
  • Hemispheric functions overstated = growing body of pop-psychology, over simplifies or exaggerates functions of hems. Hems can perform each others functions if necessary. Too simplistic.
41
Q

FMRI

A

Functional Magnetic Resonance Imaging = detects changes in blood oxygenation and flow occurring in neural activity. Active = more blood and oxygen.

42
Q

EEG

A

Electroencephalogram = electrical activity via electrodes using skull cap. records brain waves from activity of neurons. A diagnostic tool e.g. unusual arrhythmic patterns of brain activity - epilepsy, brain tumour etc.

43
Q

ERP’s

A

Event-related Potentials - extraneous brain activity filtered out from EEGs. Statistical technique, they are types of brainwave triggered by particular events - linked to cognitive processes.

44
Q

Post mortem

A

analysis of brain following death. deficit or disorder person may have suffered. Comparison too neurotypical brain in order to assess extent of the difference.

45
Q

Evaluation of FMRI

A
  • Non invasive (S) = doesn’t rely on radiation and is safe. Produces images with high spatial resolution detail shown by the millimetre. clear picture of localisation.
  • Expensive (W)= only clear picture is P is still. Poor temporal resolution 5 second lag between initial neural activity and image. not represent everyday brain activity.
46
Q

Evaluation of EEGs

A
  • invaluable in diagnosing epilepsy (s) = understanding of stages of sleep. extremely high temporal resolution. detect brain activity at a resolution of a single millisecond.
  • info received from thousands of neurons = produces generalised signal, can’t tell exactly what is being used as the source.
47
Q

Evaluation ERP’s

A
  • specific measurement of neural process (S) = achieved through raw EEG data, excellent temporal resolution, especially compared to FMRI.
  • lack of standardisation in methodology(W) = difficult to confirm findings, back ground noise and extraneous variables need to be completely eliminated. may not always be achievable
48
Q

Evaluation Post mortem

A
  • foundation for understanding the brain (S) = Broca and Wernicke relied on post mortem. Improve medical knowledge, help generate hypotheses for further study.
  • causation may be an issue = deficits may not be the cause of death. raise ethical issues of consent from patient before death. Not able to provide informed consent.
49
Q

Biological rhythms

A

periodic activity governed by;

  • internal biological clocks (endogenous pacemakers)
  • external changes in environment (exogenous zeitgebers)
50
Q

Circadian rhythm

A

Lasts 24 hours, includes the sleep/wake cycle.

51
Q

Sleep/Wake cycle

A

Exogenous zeitgebers e.g. light. Tells us when to sleep and wake up.
Endogenous e.g. biological clock. Done without the influence of external stimuli called ‘free-running’.
Governed by suprachiasmatic nucleus (SCN). receives info on light directly from optic chiasm. exogenous resets SCN.

52
Q

Siffre study

A

long period of time in cave to examine effects on free-running biological rhythms - two months in cave of southern alps, 6 months in Texan cave. settled to the usual 24 hours. did have regular sleep/wake cycle.

53
Q

Aschoff and Wever research

A

group of P’s 4 weeks in ww2 bunker without sunlight. All but one (29 hours) displayed a regular circadian rhythm. suggesting natural sleep/wake cycle may be slightly longer than 24hours.

54
Q

Folkard study of endogenous pacemakers

A

12 P’s lived in dark cave for 3 weeks going to bed when the clock turned 11;45 and waking at 7;45, gradually the clock sped up to 22 hour days. only one adjusted comfortably, rhythm cant be easily changed by external factors.

55
Q

Strengths of circadian rhythms

A
  • practical application to shift work = Boivin workers have lapse of concentration at 6am, more mistakes. Shift workers 3x more likely to develop heart disease. economic implications and better health of workers.
  • Drug treatments = CR coordinate body’s basic processes with implications for pharmacokinetics. Research = drugs more effective at certain times of day. Guidelines put in place for some drugs including cancer. Real-life medical benefits.
56
Q

Limitations of circadian rhythms

A
  • small samples = not representative of wider population limits meaningful generalisations. Rhythm slower at 60n than when younger (siffre). Even if same person factors effect study.
  • poor control = still had access to artificial light (siffre study) assumed to have no effect of free-running rhythm. Czeisler - adjusted P’s from 22 hours to 28 using dim light. could be like a drug to reset biological clocks. confounding variables limiting it.
  • Individual differences = individual cycles can vary 13 to 65 hours. Duffy, some people display a natural preference for sleeping and rising, there are opposites. Also age differences. not fully representative of population.
57
Q

Infradian rhythm

A

Female menstrual cycle 28 days. Rising levels of oestrogen cause ovary to develop and release an egg. progesterone = womb lining thickens, egg absorbed into body.

58
Q

Exogenous zeitgebers synchronising menstrual cycle

A

Stern and McClintock - 29 women irregular periods. pheromones taken from some at different stages via cotton pad under armpit, cleaned with alcohol and rubbed on to other P’s lips. 68% changed cycle to other cycle of odour donor.

59
Q

SAD infradian rhythm

A

Seasonal affective disorder - depressive disorder linked to seasons. ‘winter blues’ symptoms triggered then, shorter days. (yearly cycle). Caused by melatonin secretion for longer in winter days, leads to knock on effect with serotonin.

60
Q

Ultradian rhythms

A

Stages of sleep, 90 minute periods (more than one cycle in 24 hours). 5 stages seen by EEG.

61
Q

5 sleep stages

A

Stages 1 and 2: light sleep, easily woke, brain slower and rhythmic (alpha waves) deeper (beta waves).
Stages 3 and 4: difficult waking, deep slow sleep characterised by delta waves (greater amplitude).
Stage 5: REM (rapid eye movement) fast jerky eye activity. Body paralysed, brain activity speeds up.

Psychology A-level context + evaluation (9 decks)

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