L9: Memory and Learning

Amnesia

pathological memory loss, damaged MTL

retrograde amnesia

loss from before event

anterograde

loss from after injury

HM

MTL lobectomy + parts of amygdala and hippocampus

minor retrograde amnesia, severe anterograde

showed distinction between STM/LTM, implicit/explicit mem

HM mirror tracing test, incomplete pictures

improved but no recollection

HM verbal and non verbal matching to sample

letters were able to be rehearsed in phonological loop

non verbal lost immediately - no rehearsal

HM digit span

only remembered up to 7 digits, normal = 15

HM block tapping memory span test

up to 5, couldn’t increase to 6

MTL role in amnesia

recent memories depend on MTL to convert to LTM

MTL is not a permanent storage site

supported by monkey studies - MTL lesioned monkeys had worse performance after delays

Non MTL amnesia

Korsakoff’s syndrome, NA, Alzheimer’s, post traumatic amnesia

Korsakoff’s

degenerated diencephalon, from alcohol abuse, severe retrograde + anterograpde amnesia + sensory and motor problems, confabulation…

NA

damaged hypothalamus and mammiliary bodies

verbal deficits, couldn’t understand langauge

Alzheimer’s

basal forebrain region, neurofibrillary tangles and amyloid plaques, reduced cholinergic activity, progressive, sensorimotor learning ok

post traumatic amnesia

post concussion/coma, confusion lasts longer than coma

Non declarative memory: 2 routes

place + response strategy

place strategy

uses hippocampus, identify objects within environmental framework using landmarks, rapidly acquired + flexible

Response strategy

caudate nucleus (striatum), specific sequence of action, non declarative memory, rigid and longer lasting

Place cells in hippocampus

fire when familiar with place, each cell has field, larger hippocampi in food catching species

rat studies - rat with hippocampus damage = more errors than controls

hippocampus and spatial memory

place cells, cognitive map theory, configural association theory

cognitive map theory

hippocampus specialised for spatial location using cues

configural association theory

hippocampus is involved in long term retention of interrelations between cues

Electroconvulsive shock treatment ECS

causes graded retrograde amnesia

disruption of reverberating neural activity which prevents structural changes at synaptic level

prevents new memories right before ECS from consolidation

Long Term memory theory (Hebb)

enduring changes in efficiency of synaptic transmission = basis of LTM

learning relies on event co-occurence = progressively stronger synapses

neurons which fire together wire together

LTP

process of synaptic connections between neurons becoming stronger

growth rate = similar to learning

electrical pulse stimulating paths from pre to post synaptic neuron

LTP + memory properties

produced rapidly, lasts days/weeks, consolidation period, requires co-occuring neural activity/association of events

LTP properties

occurs in hippocampus, memory drugs affect LTP, conditioning = LTP like changes

Mechanism for LTP

Pre synaptic neuron repeatedly releases glutamate, post synaptic neuron depolarises, glutamate binds to NMDA receptors and enters post synaptic neuron, activates protein kinases = LTP

Rhinal cortex

formation of LTM explicit memories

Hippocampus

formation of spatial information

amygdala

emotion

cerebrellum

sensorimotor skills

striatum

consistent mapping

PFC

temporal order