Psychology A2

MSM explains how information flows from one store to another

seperate and permanent componants

info travels through 5 senses to sensory memory from environmental stimuli

tempo stored, limited duration, info will decay if not rehersed,  new info will displace

reharse = LTM is permantly stored, retrived at any time

milliseconds, sensory store, attention = STM.... echoic and iconic

sperlings finding of 42% and what it says about sensory memory

STM, fragile,decay easily, chuncking, displacement, limited capacity, 7 rule

peterson and peterson found after 18 sec, 3 secs and 6secs?

STM-LTM m,resharsal.. elab

LTM, distant past, gig, stored permantly, few mins-lifetime, forgetting=retrival fail

Wagner and groenwed, emotion, FBM? prisoners in camps

serial position curve, primary effect, recency effect, in the middle

clive wearing, case study problems, quantative data, why is it good?

overall eval, influential but simplistic

proposed by baddley and hitch...msm simplistic...alternative to STM

four components, C.E, PL,VSSP,EB

central exec, directs attention to part tasks, slave driver, memory determines, task allocated, cognitive tasks, no storage capacity

phono loop, audit tasks, autic control, inner ear, speech 1-2 secs.

artic control, reherses info verbally, 2 secs, repeating over and over again

VSSP, visual code, represents info, tempo stored, what it looks like, position in realtion to each other, blind person, visual cache and inner scribe

episodic buffer, general store, limited capacity,intergartion from CE and others.

dual task performance.. 2 things at once, not visual, not audit, but bother audit and visual = VSSP and PL working together, no interference.

dolcas.. brain scans, prefrontal cortex, supports, quant, sci data, objective, valid,reliable.

KF, stm and ltm work seperatly, ltm was fine, stm is damaged, audit more than visual, damage to phonological loop. supports existance of 2 slave systems.

case study criticisms... compare to multistore model.

despoito, may not be seperate in one region, many different areas, focusing on pre front cort, what about the others? mention validity.

however WMM research explained, msm not explained. doesn't over emphasis the need of rehersal. researchers agree with sub types and components.

focus on LTM,processes, increasing depth, rather than separate stores. 

non structured, memory is a result and by product of cognitive processing.

2 assump: level is effect on memory ability, deeper more long lasting traces than short

shallow, structural procces, info encoded by recog info by physical app, shape etc leads to worse recall

phonetic attends to sound of info deeper than shallow, involves maintance rehersal, short term retention

deep, semantic inv elab rehersal, more meaningful, better recall, linking knowledge with feeling. deeper= easier recall. affects how experience is stored rather than rehersal, contradicts MSM.

simplistic.

organisation, local categories, info more memorable.

distinctiveness, unusual = better recall

effort, if you have to work at it= better recall

elaboration, info is expanded to deeper level, transfer to LTM

craik and tulving found, semant words better recall, other werent, supports seman Q=Seman A. effort into visual and phonetic words

morris, phonetic, tranfer appro, other exaplanations, goes against

weakness, eyesenck said they failed to say WHY. deeper=better retention= elab. too vague and ill defined.

strengths, encoding is not simple, widened focus, it does explain why we remember.

FBM, specialised, signif inc encoded into LTM, very detailed long lasting vivid mem, not encode under normal circumtances, EG amy winehouses death. empotionally arousing, unexpected, huge significance, personal relevance. tend to be episodic rather than semantic. almost photographic detail. 6 questions....

brown and kulik..assination of black and white's emotional arousing, what it says about FBM's? andro and etho centric

ancestor history contribution, increased adrenaline production... positives of this

however Hillsborough disaster, little evidence, repression?

niesser explained by models such as MSM maintance rehersal, repeats in the media 

evidence is mixed, individual differences

frued in 1901,unconcois motivated forgetting, memories traumatic enough, not lost but repressed. this is a defence mechanism to protect concious. 

levinger and clark, recall of emotionally charged words, slow. high galvanic skin response. p's ego defenced were at work to prevent repressed words entering conscious supports repression.  objective etc, however lab.

difficult to study repression, ethical issues and cant see it happening

reduced validity of repression, not enough evidence, individual diff have diff defence mechanisms

robinson, women repress pain of childbirth over times, support fried

however not typical pain, you get something at the end of it.

frued case studies, austrian nuerotic women with anxiety. 

patients with depression have negative recall bias, more likely to recall unhappy events rather than happy ones. 

mood congruent memory

another explanation is psychical abno in brain, bio chem and structure

bower found ps tend to recall words learnt in same mood during recall. easily rep

ethics, putting someone in a bad mood

sample critisisms, not actually depressed.

relate to patients with clinical depression problems with storage, remembering personal, negative mem rather than pos

CBT, balances view of life, pos and neg, recall less depressing mems, more positive ones.

STM-trace decay, struct changes, leaves and engram, metabolic processes = breakdown unless it is reheresed. engram will disappear.

if rehersed it strengthens the connection between nuerones, 15-30secs duration and capacity is limited

forgetting is due to lack of availability

hebb suggested when learning happens, engram is very delicate and more likely to be destroyed, and with more learning and rehearsal it grows stronger

peterson and peterson...supports because trace decay led to info decaying. validity

however it could be down to displacement, new information is coming in and disrupting the engram formation.

reitman found over 15 secs p's recall was arose, evidence of trace decay. validity however displacement could of still occured 

displacement, based on limit capa of STM. new info pushes old exisiting info out when store is full. 

lack of availbility, theory suggest forgetting is due to limiting capacity, miller said 5-9 itmes. 

Waugh and Norman found recall was poor (>20%) if probe was later, recall was over 80%, supports theory of displacement, earlier numbers displaced by later ones.

however it could be down to decay. 

two types, cue external (context-dependant)= context or place where material is learnt can affect recall.

internal cues (state dependant) suggest that the physiological state of a person can affect recall.

1. evidence for external cues=godden and badly (underwater divers) results showed that words learnt and recalled in the same context were remembered better, supports. aided p's recall - the context. 

Fernandez tried to replicate and failed.

extreme environment, not everday plus P's are in their own local environment

2. evidence of internal cue's= goodwin et all found p's who hid money whilst drunk and high could find them in original state, supports. your happy when you put them away, happy when you drink or high, same mood.

plaques, tangles and granuvacuoles 

normal brains have amyloid precursor protien (APP) which can be broken down into beta amyloid 40- in normal brain

in AD brains it breaks down to beta amyloid 42, deposits build up between nuerons- plagues, cause problems between neurons. 

appear before AD symptoms, cause cerebral cortext to shrink, also causes damage to the hippocampus becuase cells are damaged in the basal forebrain which arouses cerebral cortex. AD brains are less reactive to stimuli. 

interferes with NDMA a neurotransmitter involved with learning.

Tangles, in a normal brain 'tau protein' supports structure of the cell within a neuron, when it deteriorates tangles arise where deposits of the tau protien accumulates inside the cell. this is said to be a contributing factor for AD.

Granovacuoles, abnormal appearance of small holes in cells.

autopsies show people get plagues and tangles with age but people with AD develop them at a much faster rate 

risk factors, scientist sugesst- diet etc

when all 3 have become numerous brain scans show some skrinking in the normal brain in comparison to a healthy brain.

evidence: shrinking cortex, shrunk signif hippocampus, larger ventricles

cleary said that plaques may be a cause of AD in humans, she coducted her research on rats which have a genetic link of 97.5 to humans, rats arent human = anthropomorphism. most of the work on beta-amyloid protiens has been done on animals, no animal is a perfect genetic match to a human so this could reduce the validu of P theory. dogs produce beta amyloid with age but no plagues or tangles. animals and humans are TOO different. not just biological anomloies, environmental factors such as stress? lifestyle..upbringing? cant establish cause and effect stress diathisis approach?... combined a bio with a psycho approach.

Electro-compulsive therapy is used to treat depression, passes an electric current through the brain. patient has a seizure, cannot recall events immed before treatment, explanation for this could be and increase in blood pressure in the brain and the breakdown of blood brain barrier. resulting in a hemorrhage and toxic effects, as the brain is exposed to chemicals in the blood, causes irreversible death of neurons squire and cohen found after ECT memroes for early programs remained unnaffected but after '72 recall was not as well, show LTM is affected by ECT but mainly for recent long term memories. however, deals with only one type of memory, doesnt occur in all amnesia patients = individual differences only limited for explanation of amnesia, doesnt explain why?

a neurological disorder caused by lack oh thiamine in the brain, causes irreversible damage to the hypothalamus and the cerebral atrophy. results in other retro and anterograde amnesia. the most common reason for the thiamine deficiency is chronic alcoholism, malnutrition and extreme morining sickness case study of jimmy G, still intellegance but virtually no memory retention supports, suffered both retro and anterograde amnesia, linked to alcholism vitamin difiency of brain... scientific evidence, modern brain scanning, objective, high reliability, however not a complete reason for amnesia can only explain minority.