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Multi-Store Model of Memory

Description; 3 seperate stores - Sensory Memory is always recieving information from the senses, attention must be paid to information if it is to be transferred to STM, only lasts for milliseconds and has a large capacity; Short-Term Memory lasts for around 18-20 seconds, has a limited capacity of 4-7 chunks of information, information is in a fragile state and must be rehearsed to remain in the STM or rehearsed to transfer to the LTM, information will disappear when new information enters; Long-Term Memory has unlimited capacity and unlimited duration, there is a direct relationship between rehearsal in STM and the strength of the memory in LTM.

Evaluation; Sperling used a grid of digits and letters to test SM, these were shown for 50 milliseconds and then participants were asked to recall the whole thing (5 items 42%) or 1 line (3 items 75%); Peterson and Peterson tested STM bby using 3 consonants followed by a 3 digit number, participants had to count backwards from the number and then recall the letters (3 secs - 90%, 18 secs - 2%); Bahrick tested LTM by asking a range of ages to put names to faces in their yearbooks, after 48 years they were 70% accurate. Strengths - historically important as it was the first model with testable predictions which makes this very scientific. Weaknesses - the model oversimplifies memory into only one STM store and one way of rehearsal to maintain and transfer the memories.

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Alternatives to the MSM - Levels of Processing

Levels of Processing; focused on how LTM are made, enduring memories are made through a process rather than maintenance rehearsal, some information is processed more deeply and so creates longer lasting memories, proposed that there is a primary memory where information is recirculated at a lower level of processing and more enduring memories are created by deeper processing without rehearsal memories are made through 'working over' or processing the information, early stages use analysis of physical or sensory features and the later stages use semantic analysis and comparisons to past learning. Ths hierarchy of depths of processing applies to verbal, visual and auditory information.

Evaluation; Craik and Tulving conducted a study into the different depths by giving participants common nouns and then asking questions about the noun such as 'Physical structure - Is it in capitals, Sound - does the word rhyme with train and Meaning - is the word a type of fruit?' participants remembered most words from question 3 and least form 1 showing deeper processing creates longer last memories; Mandler asked people to sort 50 cards into up to 7 piles based on any system they choose recall was greater for the most categories and poor for the least amount; Morris et al conducted a rhyming recognition test they were asked to recall words which rhymed, the best recall was for those that had not been deeply processed but phenomically processed

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Alternatives to the MSM - Working Memory Model

Working Memory Model; there are 4 components to the working memory model - Central executive has no storage capacity and directs attention to particular tasks determining how resources (slave systems) are allocated to tasks; Phonological loop deals with auditory information and preserves the order of information holds the words you hear; Visuo-spatial sketchpad is used for planning spatial tasks where the information is temporarily stored; Eposodic buffer is a general store which has limited capacity and has information from CE, PL, VSS, EB and LTM.

Evaluation; Baddeley et al showed the existence of the visuo-spatial sketchpad by giving participants a visual tracking task (track a moving light with a pointer) they had to do this whilst also completing another task (describe the F angles or perform a verbal task) this first proved difficult but not the second as it used a different slave system; Shallice and Warrington studied KF whos brain was injured a case study which shows that STM is independent from LTM as he had no problem with LT learning but some aspects of STM were impaired, forgetting for STM auditory information was much quicker than for visual, auditory impairments were limited to verbal material such as letters and numbers not meaningful sounds which suggested that the phonological loop was affected; only looks at STM so it is a very limited model of memory, the number of stores are poorly defined for example critics believe there are severa CE's not just one.

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Role of Emotion in Memory

Enhanced Memories; Flashbulb memories are similar to a picture of a specific time, place and the people you were with, usually centered around an important event such as the death of Princess Diana or 9/11 or an injury or personal events. Evaluation; Wright interviewed people about Hillsborough after 5 months people had no FBM, they had reconstructed memories based on other peoples recall; Conway et al looked at cultural differences in FBM, found 86% of UK participants had FBM of Thatchers resignation 11 months after but only 29% in other countries.

Imparied Memory; Repression; proposed by Freud this is a method which the ego uses to protect itself from emotional conflicts such as when something traumatic has happened, to avoid anxiety it is repressed (placed beyond consciousness) anxiety is later expressed through dreams such as in Little Hans. Evaluation; Williams used 206 cases of childhood sexual assault and interviewed 129 of the victims around 20 years later over a third (38%) of the women did not recall the sexual absue and of those who could 16% sasid at one point they couldnt but had recovered the memory; there is also event specific amnesia during which we repress certain events these events are then retrieved through therapy. Depressive state; creates a negative recall bias in which the persons remembers only unhappy and negative events (mood dependant memory causes us to link similar moods) depression causes people to be inattentive and so they dont create new LTMs. Evaluation; 174 adults with depression were asked to complete memory tasks scored poorly, when retested after 6 months of treatment they scored better.

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Explanations of Forgetting - STM

Decay theory; we have a physical representation of a memory in the brain and it is suggested that this trace simply disappears or decays if it is not rehearsed (which would strengthen connections between neurons) for example in Peterson and Peterson no rehearsal was permitted and so the memory was lost after 18 seconds. 

Displacement theory; a set of new information simply overwrites the current information in the STM as it has a limited capacity of 4-7 chunks. 

Decay or Displacement?; Peterson and Peterson shows that decay theory happens after 18 seconds however it is possible that the information did not decay but was displaced by the numbers; Waugh and Norman presented 16 numbers to participants if the probe was early on the list the recall was poor (less than 20%) whereas if the probe was near the endof the list the recall was good (over 80%) this supports displacement as the new numbers replace the older ones, however if the speed of presentation is altered there is some evidence for decay, if the numbers were presented 4 per second the recall was better than if they were presented 1 per second as they had less time to decay; Shallice found that forgetting was reduced if the numbers were presented faster but found a stronger effect for moving the position of the probe this suggests that displacement is more important than decay.

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Explanations of Forgetting - LTM

Decay; LTM decay may be due to physical decay ie. brain damageInterference; Proactive interference means that an old memory interferes with current attempts to learn something; Reteroactive interference is when current memories interfere with past learning; Underwood showed evidence for both PI and RI - participant must learn a list of word pairs (List A and List B) and then is required to learn a second list (List A and List C) the participant is given the first word of the pair and asked to recall List C (PI) or List B (RI)Cue-dependent Forgetting; mainly due to retrieval failure as you dont have enough clues or cues; External cues are a specific room, person or item whereas Internal cues are mood dependent (drunk or sober, or excersising or not excersising) these affect our ability to remember tasks we completed while in that state.

Decay or Inerference? Baddeley and Hitch looked at whether rugby players who played all fixtures remembered less than rugby players who missed some fixtures due to injury; if decay theory is correct they should remember a similar percentage each; if interference is correct the players who played in the most games should forget due to interference - this is what they found. Interference or Cue-dependent?  Interference only explains part of forgetting; Tulving and Psotka gave participants 6 word lists of 24 words in 6 categorgies to learn, participants were asked to recall as many words as they can and then recall a specific category some learning 1 list, some 2 and so on, the more lists they learned the less they remembered(RI) however during cued-recall the effects of interference disappeared showing that interference masks memory.

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Disorders of Memory - Amnesia

Loss of explicit memory; explicit means that the information can be deliberately and consciously recalled, implicit means recollection is independent of conscious awareness. Schacter said that forgetting in Amnesiacs could be explained by impaired explicit memory as many perform better on tests of implicit memory (tasks where thye demonstrate learning through behaviour) eg in HM. Procedural memory is knowing how and declarative is knowing what.Evaluation; Stickgold found amnesiacs can improve at Tetris but have no memory of doing so or how to play it; Schater found representing words in the same voice as learned in helped normal memory but not amnesaics; Ryan says that amnesiacs fail to recall the links between implicit and explicit aspects of events.

Inability to consolidate new memories; Anterograde amnesia is the inability to form new LTMs, this may be due to problems with consolidation or retrieval of memories, Isaac and Hayes found that amnesiacs performed as well as controls on cued recall and recognition tests suggesting the problem is with consolidation not retrieval. Reterograde amnesia is the loss of memory for past events, recall is worse for events occuring around the time of the onset of the amnesia recall of older events increases with more time, associated with damage to the hippocampus. Evaluation; many have both RA and AA, damage to only part of the hippocampus caused only AA; Reed and Squire found damage to the temporal lobe caused worse symptoms; Remondes and Schman lesioned rats hippocampus and showed they could learn a maze but forgot it quickly suggesting they could make new memories but not consolidate them.

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Disorders of Memory - Alzheimers Disease

B-Amyloid and Plaques; normally B-amyloid 40 is produced but in AZ B-amyloid 42 is produced, this builds up between neurons and creates plaques, these start to form before the symptoms of AZ appear but they progess causing the Cerebral cortex to shrink; cells in the basal forebrain are also damaged causing low alertness; B-amyloid also interferes with NDMA which normally helps produce changes in the synapses that produce long-term potentiation (changes linked to learning). Tangles; formed by a build up of tau protein which arise when the cell body degenerates. Evaluation; difficult to see how plaques are a cause of AZ; Murphy and LeVine say this is due to B-amyloids creating a chain which progresses irrespective of B-amyloid levels; Animal studies are used throughtout AZ but no species has the same symptoms as humans developing little nerve damage meaning generalisations from animals too humans may not be valid.

Genes; Lott noticed that people with Downs syndrome developed ealry onset AZ, this lead to the link between the extra chromosome 21 and AZ, other genes have been found on chromosome 1 and 14. Genes with later onset AZ are found on chromosome 10, these genes produce more B-amyloid. Evaluation; around half of AZ patients have no known relatives with AZ suggesting small genetic influence however there are genes associated; Yoruba people suffer less from AZ despite similar genes which shows that other factors influence the onset of AZ such has high salt, fat and calories in diets; genes influence the production of B-amyloid and tau proteins, B-amyloid treatments to block production reduce deteriation in memory.

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