13/01/2022 PY2CBP – Lecture 1 cognitive and biopsychology
Biopsychology – biological approach to the scientific study of behaviour
Includes: cognitive neuroscience, neuropsychology, comparative psychology etc.
Cognitive psychology – scientific study of behaviour when performing cognitive tasks
Inference of healthy individual’s conditions based on performance of brain damaged Ps
Includes: computational cognitive science, cognitive neuroscience, cognitive neuropsychology etc.
Cognitive psychology strengths = double dissociation evidence, transformed lang research
Cognitive psychology limitations = many over specific, contradictory, theoretical models
Assumptions in cognitive neuroscience
Modularity – aspects of cognition are independent
Subtractivity – damage impairs one area and leave others in tact
Transparency – changes in model mimics changes in real person
Cognitive neuroscience strengths = variety of techniques offering spatial or temporal resolution
Cognitive neuroscience limitations = activity is not causation & variability in analysis of data
17/01/2022 PY2CBP – Lecture 2 chemistry of behaviour
Neurotransmitter are synthesised in cytoplasm in the terminal button
Exocytosis – ion channels open when stimulated by AP membranes
Agonists: produces the same action as NT v antagonists: prevents the action of NT
Drug efficacy: time spent being bound (e.g. low = uncouples quickly, need higher concentration)
Agonists: high efficacy (do what NTs are supposed to do) & antagonists: low efficacy
Drugs can affect any stage in syntactic transmission: block receptors, prevent reuptake, leak vesicles
Enzyme mechanism in the presynaptic regulates NT overproduction by making some inactive
Classical antipsychotics: based on the dopamine hypothesis & effective in alleviating + symptoms
Neuroleptics target the mesolimbic (midbrain to limbic system) pathway: block D2 receptors
, Other DA pathways are also affected, which is what causes side effects ( - symptoms) = ‘dirty’ drug
Atypical antipsychotics: binding takes place at serotonin sites, weaker dopamine antagonism,
alleviated + & - symptoms, shorter bind to D2 receptor, fewer side effects
Need to balance serotonin against dopamine antagonism (contradicts dopamine hypothesis)
Monoamine oxidase inhibitors (antidepressants): prevents breakdown of monoamines = DA, 5-HT &
noradrenaline -> severe side effects & can have dietary restrictions (cheese, beer)
Tricyclics: prevented 5-HT reuptake = can cause cardiovascular side effects
SSRIs: less side effects than older drugs
Anxiolytics: CNS depressants with widespread effects: decrease consciousness (dangerous OD)
GABA agonists = GABA is inhibitory, reduces chances of AP & decreases excitability
Opioids = relieves pain but addictive drugs interact with DA/reward pathways
Naturally occurring opioids like NT e.g. endorphins = agonists on opioid receptors
Reduces pain by making AP less likely or making the presynapse less likely to release NT
24/01/2022 PY2CBP – Lecture 3 attention and consciousness
Restraints on attention = only a minority of neurons can be highly active at once
Two systems of attention = endogenous (selective attention) & exogenous (hijacks attention)
Cocktail party effect = noisy environment causes selective auditory attention, but some unattended
info can break through (your name)
Lab methodology = simultaneous dichotomous stimulus presented, told to focus on one then tested
on recall of the ignored stream = could recall physical properties (tone, pitch change) but no content
or language change detected
Broadbent’s filter theory model = early filter, initial parallel processing (extract all physical
properties) then serial processing (decode a stream at a time)
Explains cocktail party effect, supporting evidence that recall from non-attended channel is limited
Attenuated filter theory = early filter but less strong, meaningful stimuli can break through so non
attended info is not completely filtered out (explains break through stimlui)
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