Biopsychology - ALL

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191 Terms

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Biological Rhythms

What are biological rhythms?

Distinct patterns of changes in body activity that relate to cyclical time periods/changes in environment

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Biological Rhythms

What are the 3 types of biological rhythm?

Circadian

Infradian

Ultradian

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Biological Rhythms

What are the rhythms controlled by?

Endogenous pacemakers

Exogenous Zeitgebers

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Biological Rhythms

What are endogenous pacemakers?

Mechanisms within the body that govern internal biological rhythms

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Biological Rhythms

What are exogenous zeitgebers?

External changes in the environment

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Biological Rhythms

What are circadian rhythms + example?

Approx. 24 hour duration

eg: sleep/wake cycle

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Biological Rhythms

How do endogenous pacemakers control circadian rhythm (sleep/wake cycle)?

  • Suprachiasmatic nucleus (SCN) - connected to visual cortex and receives info about light

  • Pineal gland - releases melatonin which induces relaxation (sleepy)

  • Adrenal gland - releases cortisol which induces alternes (wakes up)

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Biological Rhythms

DeCoursey et al (2000) - EP circadian

destroyed SCN connections in brains of 30 chipmunks who were then returned to natural habitat for 80 days

found: sleep/wake cycle disappeared, awake same time as predators (died) → supports idea of EP controlling circadian rhythms

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Biological Rhythms

Siffre case study - EP circadian

  • caves: 2 months in alps + 6 months in Texas

  • in absence of natural light, sleep/wake cycle was 25 hours

  • suggests endogenously controlled as cycle similar length

Issue: had artificial light

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Biological Rhythms

How do exogenous Zeitgebers control circadian rhythm?

Light - provides info for SCN

Social cues - eg: meal times, clocks

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Biological Rhythms

Campbell and Murphy (1998) - EZ circadian

  • woke 15 participants at various times and shone a light on the back of their knees

  • produced a deviation of the usual sleep/wake cycle by up to 3 hours

Issue: findings never been replicated, small sample

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Biological Rhythms

What are ultradian rhythms + example?

Duration of less than 24 hours
eg: sleep cycle

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Biological Rhythms

How do endogenous pacemakers control ultradian rhythms?

5 sleep stages that span 90mins

1+2 = light sleep, easily woken, brainwaves become slower + more rhythmic, slowing further as sleep becomes deeper

3+4 = difficult to rouse, deep sleep, slow waves with great altitude

5 = REM (rapid eye movement) sleep, brain activity speeds up

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Biological Rhythms

What waves are produced in each stage?

1 + 2 = alpha waves + beta waves

3 + 4 = delta waves

5/REM = alpha waves

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Biological Rhythms

Dement - EP ultradian

Used EEG

Found dreaming correlated with REM activity in 9 participants

Issue: population validity + correlational

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Biological Rhythms

What does BRAC stand for?

basic rest activity cycle

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Biological Rhythms

BRAC - EP ultradian

  • Kleitman referred to 90min cycle found during sleep as BRAC

  • move through stages of alertness, not sleep

  • only can concentrate for 90mins

  • towards end we fatigue, lose resources and concentration

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Biological Rhythms

What are infradian rhythms + example?

Duration greater than 24 hours
eg: menstrual cycle

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Biological Rhythms

How do endogenous pacemakers control infradian rhythms (menstrual cycle)?

  • controlled by changes in hormone levels which regulate ovulation

  • during each cycle there is an increase in oestrogen/progesterone/FSH/LH

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Biological Rhythms

(EVALUATION TOO) Stern and McClintock (1998) - EZ infradian

  • samples of pheromones taken from 9 women by cotton pads under pits for 8 hours

  • treated and given to other ps by rubbing pad on upper lip

  • 68% experienced changes in cycles to be closer to their 'odour donor'

Issue: Trevathan et al (1993) didn't get same results → low reliability

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Biological Rhythms

Seasonal affective disorder - EZ infradian

  • depression experienced in winter

  • main symptom is low mood

  • lack of light in winter = melatonin produced for longer, knock on effect on production of serotonin

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Biological Rhythms

CR Evaluation: Siffre

Siffre found without natural light, his sleep/wake cycle only shifted to 25 hours (supports the idea that EPs = more important to the circadian rhythm) BUT low validity bcs artificial light/clock extraneous variables (EZs - social cues)

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Biological Rhythms

CR Evaluation: Idividual differences

eg: age, effect CRs → adolescent's sleep/wake cycles appear to = 2hrs later vs adults → research in school that started lessons at 10 = positive health/academic outcomes → LIMITATION OF NOMOTHETIC APPROACH BCS NOT ALL LAWS APPLY EQUALLY TO EVERYONE

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Biological Rhythms

CR Evaluation: alt explanation to light

Buhr et al (2010) suggests temperature controls body clock + light = trigger, bcs SCN transforms info about light -> neural messages that set body temp -> fluctuates over 24hrs -> controls body clock

BUT need more research

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Biological Rhythms

CR Evaluation: Low validity of isolation studies

V rare for EPs to be free-running/unaffected by EZs so isolation studies like Siffre (since been questioned) are rare, and it might make little sense/have little validity to try to isolate them

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Biological Rhythms

CR Evaluation: Practical application

negative impacts of desynchronisation (eg: shown that shift workers more likely to develop heart disease, lowered vigilance, more anxiety) can have economic impact by managing worker productivity

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Biological Rhythms

CR - what is desynchronisation?

disrupting the rhythm so that EPs and EZs are no longer working in synchrony

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Biological Rhythms

UR Evaluation: Supporting research

Tucker et al (2007) found 21 Ps over 11 days/nights found large significant differences in sleep duration/time to fall asleep/time in each sleep stage, meaning differences b/w people may be due to biology, not just circumstance.

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Biological Rhythms

UR Evaluation: limitation of support

Tucker et al (2007) had a small sample size (21) meaning it's hard to generalise to the gen pop because they may not be representational (population validity).

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Biological Rhythms

UR - Practical application

Understanding sleep cycle can be used in everyday routines to make lives easier - Believed 5 stages of sleep cycle take 90 mins, so if timed to wake up in first 2 stages will be more easily woken + feel more awake

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Biological Rhythms

EP/CR Evaluation: Supporting research

Decoursey et al (2000) found when severed 30 chipmunks SCNs pathways + re-released them, most died bcs sleep/wake cycle changed + awake at same time as predators, supporting the idea that EPs play a role in maintaining our CRs

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Biological Rhythms

EP/EZ/CR Evaluation: Supporting research issue (animal studies)

DeCourset et al (2000) used chipmunks to research effect of the EP SCN on the CR, yet generalised to humans BUT can't extrapolate results to humans bcs brains = more complex so can't assume will have same effect, so animal studies are limitations for research into EPs/EZs

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Biological Rhythms

EZ/UR Evaluation - Small sample

Sleep studies generally have small sample sizes, (eg: Campbell + Murphy (1998) = 15 Ps to study effect of light on sleep cycle) so lack pop val bcs can’t be representative, lack generalisability

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Biological Rhythms

EZ/EP/UR Evaluation: Practical application

Treatment for SAD = Phototherapy (light box simulates strong morning/evening light to reset melatonin levels - relieves 60% of symptoms (but placebos can have similar effects)) means melatonin levels increase, cortisol increase → boosts energy and increases serotonin (therefore increase mood)

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Biological Rhythms

EPs/EZs Evaluation: I + D nature-nurture

follow on from low validity of isolation studies point

EPs = nature, EZ = nurture

EPs (eg: hormones) are internal factors (biological), and EZs (eg: light) are external factors (environment) so support interactionalist approach to nature-nurture debate

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Neurons + synaptic transmission

what are excitatory neurotransmitters?

  • eg: noradrenaline

  • increase the likelihood of an impulse being transferred to the postsynaptic neuron

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Neurons + synaptic transmission

what is excitatory post-synaptic potential (EPSP)?

  • What an excitatory neurotransmitter bonding with a postsynaptic receptor results in

  • Means the postsynaptic cell is more likely to fire

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Neurons + synaptic transmission

what are Inhibitory neurotransmitters?

  • Eg: serotonin and GABA

  • decrease the likelihood of the presynaptic neuron firing

  • They calm the mind and the body

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Neurons + synaptic transmission

what is inhibitory post-synaptic potential (IPSP)?

  • What an inhibitory neurotransmitter bonding with a postsynaptic receptor results in

  • means the postsynaptic cell is less likely to fire

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Neurons + synaptic transmission

What is whether the cell fires or not determined by?

  • sum of the excitatory (+) and inhibitory (-) inputs

  • because a nerve can receive bother EPSPs and IPSPs at the same time

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<p><strong>Neurons + synaptic transmission</strong></p><p>What will the overall effect be on this nerve?</p>

Neurons + synaptic transmission

What will the overall effect be on this nerve?

excitatory

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<p><strong>Neurons + synaptic transmission</strong></p><p>What’s a Motor Neurone?</p>

Neurons + synaptic transmission

What’s a Motor Neurone?

Send impulses from the brain to the muscles/effectors

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Neurons + synaptic transmission

What’s a neurotransmitter?

Chemical substances that transmit nerve impulses across a synapse

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<p><strong>Neurons + synaptic transmission</strong></p><p>What’s a Relay Neurone?</p>

Neurons + synaptic transmission

What’s a Relay Neurone?

  • Allow sensory and motor neurones to communicate

  • found in the brain and CNS

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<p><strong>Neurons + synaptic transmission</strong></p><p>What’s a Sensory Neurone?</p>

Neurons + synaptic transmission

What’s a Sensory Neurone?

Carry nerve impulses from sensory receptors to the spinal cord and the brain

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Neurons + synaptic transmission

What’s a Synapse?

an area where 2 neurons come close enough to each other to pass chemical signals from one cell to another

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<p><strong>Neurons + synaptic transmission</strong></p><p>What are Axon terminals?</p>

Neurons + synaptic transmission

What are Axon terminals?

  • The end of the neurone

  • synaptic transmission occurs

  • the signal is passed to the next neuron

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<p><strong>Neurons + synaptic transmission</strong></p><p>What are <span style="font-family: Aptos, sans-serif">Schwann cells?</span></p>

Neurons + synaptic transmission

What are Schwann cells?

  • made of myelin sheaths

  • Insulates the axon so the electrical impulses can travel faster

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<p><strong>Neurons + synaptic transmission</strong></p><p>What’s a Cell body/stoma?</p>

Neurons + synaptic transmission

What’s a Cell body/stoma?

Stores the Nucleus

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<p><strong>Neurons + synaptic transmission</strong></p><p>What’s a dendrite?</p>

Neurons + synaptic transmission

What’s a dendrite?

receives signal from other neurons or from sensory receptor cells

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Neurons + synaptic transmission

what are axons?

carry nerve impulses away from the cell body towards the axon terminals

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Neurons + synaptic transmission

what are the qualities of a sensory neuron?

  • send information from the senses to the brain

  • short axons

  • long dendrites

  • cell body in the middle

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Neurons + synaptic transmission

what are the qualities of a relay neuron?

  • mostly found in the brain/CNS and act between the sensory and motor neurons

  • long or short axon

  • short dendrites

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Neurons + synaptic transmission

what are the qualities of motor neurons?

  • send messages via long axons from the brain to the muscles of effectors

  • long axons

  • short dendrites

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Neurons + synaptic transmission

What’s Synaptic transmission?

process where a nerve impulse passes across the synaptic cleft from one neurone (the presynaptic neurone) to another (the postsynaptic neurone)

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Neurons + synaptic transmission

what is reuptake?

after the impulse has been transferred any left over neurotransmitters are reabsorbed by the presynaptic neuron and stored for later impulses

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Neurons + synaptic transmission

What is the first stage of synaptic transmission?

an electrical impulse (the action potential) travels down the Pre-synaptic axon terminal

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Neurons + synaptic transmission

What is the second stage of synaptic transmission?

Impulse triggers the vesicles bind with its membrane and release the neurotransmitters into the synaptic cleft

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Neurons + synaptic transmission

What’s the third stage of synaptic transmission?

the NTs diffuse across the synaptic gap where it binds to specific receptors on the surface of the postsynaptic neuron and triggers the action potential increase/decrease likelihood

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Neurons + synaptic transmission

What’s the fourth stage of synaptic transmission?

the neurotransmitter are taken out of the synapse in 're-uptake'

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Neurons + synaptic transmission

What’s a vesicle?

Small sacs in the pre-synaptic neurone that contain neurotransmitters

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Neurons + synaptic transmission

What are ways the NTs may leave the synaptic cleft?

  • digested by enzymes and components used to make more NTs

  • taken back into presynaptic neurone via reuptake

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Lateralisation

What is it called when one hemisphere is responsible for the other side of the body’s functions?

contralateral

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Lateralisation

What is lateralisation?

theory that two brain hemispheres are functionally different + certain processes/behaviours are mainly controlled by one hemisphere over the other

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Lateralisation

What hemisphere is visual centre in?

Both

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Lateralisation

What hemisphere are the language centres in?

left

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Lateralisation

What are the two hemispheres of the brain connected by?

Corpus callosum

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Lateralisation

AO1 - what is the surgery that cuts out the corpus callosum, creating split brain patients?

commissurotomy

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Lateralisation

Who did Sperry's experiment involve?

  • 11 split brain patients who had commissurotomy

  • meant could research the extent to which each hemisphere was specialised + which brain functions were lateralised

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Lateralisation

Sperry’s procedure:

RVF = right visual field

LVF = left visual field

  1. image/word shown to RVF + same/different image/word shown to LVF (done by covering one eye + flashing the image/work for 1/10 of a second)

  2. SO, patient could only process w/ one hemisphere

  3. some trials had objects under a table they were allowed to touch

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Lateralisation

Sperry’s findings:

  • Could describe what they saw if projected to RVF

  • Unable to do describe if projected to LVF, but could draw w/ left hand

  • Could attach verbal labels to objects presented to RVF

  • COULDN’T if presented to LVF, but could select relevant corresponding object from bag using left hand - eg: if shown a cigarette, picked up ash tray - (recognition by touch)

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Lateralisation

Explain Sperry’s findings

L/RH = left/right hemisphere

  • Broca’s area (lang production) and Wernicke’s area (lang comprehension) = LH

  • LH controls right side of body + vice versa (is contralateral)

  • SO, patients couldn’t describe what was seen in LVF bcs processed by RH, so no lang centres

  • COULD draw/pick up w/ left hand bcs also controlled by RH → PROVES the RH was processing the info even though couldn’t verbalise it

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Lateralisation

Evaluation: Supporting research

Sperry produced evidence that LH = associated w/ lang + analysis, RH = associated w/ emotion + synthesising info, + motor functions = contralateral → contributed to understanding of how the brain works + suggests certain functions are lateralised

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Lateralisation

Evaluation: well controlled/replicability

Sperry’s methodology ensured info was only being received by 1 hemisphere (controlled) and was replicable→ meant could be confident in his conclusion about hemisphere laterisation bcs of well-controlled + useful procedure

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Lateralisation

Evaluation: representation

Split brain patients are abnormal - all of Sperry’s Ps had history of epileptic fits, unique brain trauma bcs of commissurotomy, sample = 11 → conclusions need caution as unlikely to be completely representative of general population (lacks pop val)

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Lateralisation

Evaluation: lab study

Lacks mundane realism (how well the experiment represents/mimics real life) → artificial task to cover eyes + look at images for 1/10 seconds → SO lacks generalisability to real life

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Lateralisation

Evaluation: oversimplified

Sperry’s research led to growth in research that oversimplified/overemphasised lateralisation BUT hemispheres = in constant communication + research into neural plasticity/functional recovery (eg: Jody Miller - RH removed, but still able to use both side of body as if hadn't) demonstrates functions associated w/ one hemisphere can be effectively performed by other

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Lateralisation

Evaluation: practical application

Rogers et al (2004) found lateralisation = associated w/ enhanced neural processing capacity (performing multiple tasks simultaneously) in chickens (eg: finding food + being vigilant for predators) → demonstrates how brain efficiency can be maximised in cognitive tasks

BUT issues w/ extrapolation from chicken’s → complex human brains

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What are the 4 ways of studying the brain?

  • post mortem examinations

  • EEG

  • ERPS

  • fMRI

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  1. what are post mortem examinations?

  2. what are they used for?

  1. Involve dissecting the brain of a person who has died - can be comparing brain w/ disorder and ‘normal’ brain

  2. to establish the underlying neurobiology of a particular behaviour

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Why would post-mortem examinations be used?

What do they show?

  • to physically look at the internal structures of the brain

  • only way to study brain before modern brain scanning techniques

  • structural abnormalities that may explain disorders (Brown et al (1986) - schizophrenic patient had enlarged ventricles in brain)

  • Evidence for localisation (eg: Broca - 2 patients w/ speech production issues both had damage to same area (Broca’s area)) (Annese et al - HM’s inability to store new memories bcs of damaged hippocampus)

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What are the pros of post-mortem examinations?

  • Allows for more detailed examination - couldn't be done while alive bcs too invasive

  • vital in early understanding of key processes in the brain (Broca + Wernicke both relied on PM examinations for research)

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What are the cons of post-mortem examinations?

  • People die in a variety of circumstances/varying stages of disease which can influence the brain post-mortem - Eg: drug treatments, age, and time b/w death and examination are all confounding variables - so cause and effect cannot be confidently established

  • Small sample sizes → lack validity

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What are fMRIs?

What are their uses?

Functional Magnetic Resonance Imaging scans are 3d scans that show changes in brain activity as they happen

Localisation of Function

Shows damaged/diseased areas of brain → diagnose medical problems

Study abnormal activity → Shegill et al (2001) show areas active for patient’s schizophrenic hallucinations

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How do fMRIs work?

  • Magnetic field + radio waves

  • oxygenated blood react differently to magnetic field than deoxygenated

  • active areas of the brain require oxygenated blood

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What are the pros of fMRIs?

  • Non-invasive -> doesn't rely on radiation

  • Has good spatial resolution (it produces images that depict detail by the mm so gives a clear pic of how activity is localised)

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What are the cons of fMRIs?

  • Can only measure blood flow -cannot hone in on activity of individual neurons so difficult to tell what kind of activity is being shown - not truly quantitative measure

  • expensive compared to other neuroimaging techniques → small sample sizes → issues w/ generalising research

  • poor temporal resolution → 5s time lag after neural activity

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What are ERPs?

  • Biopsychologists look at how an EEG wave pattern changes in response to a stimulus

  • This is known as an event-related potential

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How are ERPs detected?

  • if a specific stimulus is presented, it produces a specific change in the wave pattern

  • Biopsychologists have identified different ERPs that are produced in response to different stimuli

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What are uses of ERPs?

  • Used a lot in memory research - give biopsychologists clues to information processing in the brain

  • Research has shown differences in ERPs of people w/ certain disorders compared to healthy individuals (eg: Miltner et al (2000) - people w/ phobias had an ERP of a greater amplitude in response to objects they feared, compared to non-phobic individuals

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What are the pros of ERPs?

  • (same of EEGs)

  • Provides specificity to the measurement of neural processes compared to EEGs

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What are the cons of ERPs?

  • (same of EEGs)

  • Needs to be repeated many times for an average - time consuming

  • Often difficult to pick out from other electrical activity - so a large number of trails have to be conducted

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What are EEGs?

How do they work?

  • An electroencephalogram shows the overall electrical activity of the brain

  • done by placing electrodes on scalp, when neurones fire they produce electrical fields which are recorded as brain waves, more electrons = stronger fields

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what are the uses of EEGs?

  • Dement (1957) - correlated REM activity + dreaming

  • study schizophrenia (eg: Boutros et al (2008) meta-analysis - patients displayed abnormal EEG wave patterns compared to controls)

  • abnormal brain activity can show if person having seizure is epileptic

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What are the pros of EEGs?

  • Non-invasive

  • Cheaper than fMRIs - can be more widely used in research - larger sample sizes/more confident generalisations

  • Useful in clinical diagnostics

  • high temporal resolution - detects activity within millisecond

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What are the cons of EEGs?

  • Low ecological validity bcs in lab where (eg) sleep behaviours may not be the same as at home or a familiar environment

  • Poor spatial resolution - only provide generalised information - difficult to pinpoint the source of any activity if the locations are neighbouring

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What’s the difference in EEGs and ERPs?

In an ERP a stimulus is presented to the P and the researcher looks for activity related to that stimulus

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Localisation

what does anterior mean?

towards the front

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Localisation

what does posterior mean?

towards the back

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Localisation

what does superior mean?

above