Memory Flashcards
Key terms learning memory recall the engram
- acquistion of info
- storage of learned info
- reacquisition of stored info
- physical embodiment of memory
Forms/ Types of memory
Independent memory systems?
- procedural/ declarative
-nervous systems perform different types of learning/memory
-procedural vs declarative = implicit vs explicit
p= skills and associations largely unavailable to conscious mind (eg. motor memory)
d= available to conscious mind- can be encoded in symbols and language
Memory duration
immediate memory - few seconds
STM - seconds or minutes = working memory here
LTM- days, years
Important structures:
- pre-frontal cortex
- hippocampus
- amygdala
- cerebellum
- working
- essential for converting STM to LTM, declarative memory
- multiple, processed sensory inputs(smell), implicit/emotional/ learnt fear
- motor control and learning= procedural, sensorimotor
Hippocampus
-lesions?
inputs from where?
outputs via where?
hippocampal lesions (elective or accidental) cause memory loss
stroke in hippocampus = memory loss
-3-layered cortex
-unusual development(due to external surfaces fusing as they curl round)
–>CA fields 1, 2 ,3 ,4
-inputs from entornial cortex and beyond
-outputs to many regions via fornix
Mechanisms of memory
reverberating circuits?
hebbian synapse concept?
memory and synaptic plasticity?
LT facilitation/ depression?
long term storage appears to be distributed across the brain(more to do with connections)
Reverberating circuits = memories are disributed over many cells
The hebbian synapse concept - synapses could be changed due to activity being modificable
–>memory and synaptic plasticity
-synaptic strength changes
-facilitation/depression (synapse) –can be ST, Ca++availability/vesicle depression effects efficiency of synapse
(depression=produces lower response with same input)
-Long-term facilitation/depresion
Long-term potentiation
what is it?
where?
What is Post-tetanic?
LTP in hippocampal slices(and elsewhere in brain also)
- LTP was looked at between CA1 and CA3, by looking at strengthening response from CA1 (do this via stimulation)
- Post-tetanic LTP = give big stimulus,then smaller one, post-tetanic LTP happens after the high frequency burst
What is paired LTP?
-coincident stimulus and depolarisation
2 inputs to same cell at same time= stronger response later on from cell = shows associativity
Long term depression?
where?
what is it?
in cerebellum
=its a smaller response than before(weakening the response from the synapse)
(if this was to be an inhibitory synapse= could cause increase in activity overall)
Aplysia Californica - gill withdrawal reflex in siphen
shows?
gill withdrawal reflex
Shows: habituation,
short term sensitisation:
– repeated gentle stimulation to siphen causes reduced gill withdrawal = habituation
–but if you pair single tail pinch(aversive) with siphen touch = re-establish siphon reflex
long term sensitisation:
–repeated pairing of siphen touch and tail pich
–LT, non-habituating siphen
classical(Pavlovian) and operant(skinner) conditioning
Common themes between LTP, LTD and aplysia
- all require receptor activation(glutamate/ serotonin)
- altered synaptic responsivity
- mediated by second messengers (Ca++/ cAMP)
- require protein phosphorylation changes in early stages
- require protein synthesis for late stages of memory formation (due to need for structural change)
- involve biochemical and structural pre and post-synaptic changes
Pathologies affecting memory? Anterograde amnesia? Retrograde amnesia? causes? Alzheimers?
forgetting allows for more important things to be focused on and remembered
pathological forgetting= amnesia
Anterograde amnesia = problem forming new memories
Retrograde amnesia = problem remembering old memories
can be caused by: head injury, tumour, surgery, ECT
Alzheimers - hippocampal susceptibility
AD brain - senile plaques and tangles
-taxi drivers = better hippocampus study
