l5- how many types of memory r there? Flashcards
william james on memory 1890
- distinguished between primary n secondary memory
- primary: doesnt survive the instant of passage
- secondary: lasts a few moments, hours or days
- some memories leave indestructible vestiges (habits?)
lashleys law of mass effect 1931
- ’ the degree of memory deficit seems proportionate to the amount of tissue destroyed, irrespective of the locus of the injury’
atkinson + shiffrin multistore model 1966
- suggests serperation between long n short term memory
- supported by H.M
case of HM
- underwent bilateral medial temporal-lobe resection
- resilted in profound anterograde amnesia
- couldnt form new memories, partial retrograde amnesia
- retained early childhood memories
- IQ=112; memory quotient= 67- IQ average is 100
- intact STM(up to 40 secs)
- mirror tracing ability intact (milner 1962)
frontal lobe n working memory (owen et al 1990)
- FL patients impaired at organized search
- more errors under high load
- wm depends on prefrontal cortex
neurochemsitry n wm
- persistent activity maintains info (fuster 1972)
- dopamine, noradrenaline, serotonin systems involved
- dopamine depletion impairs wm (brozoski et al 1979)
we have diff neurochemical systems in the brain
1) Different neurotransmitter systems project to different brain regions
2) Each neurotransmitter can bind to specific types of receptors ( ASIDE: Dopamine = 5, Serotonin = 14. Noradrenaline = 9).
effect of methylphenidate
mehta et al 2001
- imporves wm
- increase dorsolateral PFC activity
- works by blocking dopamine n noradrenaline reuptake
LTM is not unitary
- includes declarative n non-declarative memory
- involves hippocampus, pFC n striatum
weather predicition task
knowlton et al 1994+1996
- amnesic patients can learn probablisitic associations
- parkinson pts cannot learn habits but can retain knowledge
- double dissociation: hippocampus vs striatum
priming
warrington + weiskrantz 1970
- amnesic pts show intact priming despite poor recall
- recognition from degraded words preserved
- priming doesnt require hippocampus
priming n the brain
schacter et al 1996
- used PET w radiolabelled CO2
- explicit memory experiment
- semantic (high recall)-‘name as many words associated w’. s
- reduced blood flow in visual cortex for primed words
- no change in hippocampus
- priming= implicit memory
explicit memory + semantic encoding (schacter et al 1996)
- semantic encoding increases posterior hippocampus acitivity
- non-semantic encoding increases Left PFC activity and precuneus (KEY: L/R r flipped in pfc)
what brain regions show more actiivty during semantic encoding?
- l+r posterior hippocampus
- = HC is argued to be involved in conscious recollection
what brain regions show more activity for non-semantic encoding?
- precuneus (medial parietal lobe)
- left prefrontal cortex (L/R=flipped)
emotional memory n the amygdala
bechara et al 1995
- examind effects of lesions to HC,AG or both. habitatgional phase then learning phase. controls showed expected skin responses (SCR) and conscious recollection
- hippocampul damage: no conscious recollectation but normal emotional response
- amygdala damage: no emotional but preserved memory
- both damaged: no response no recollection
- emotoional learning measured via skun conductance response (SCR)
final summary
- memory involves multiple regions:
- hippocampus
- striatum
- neocortex
- amygdala
- prefrontal cortex
