Learning and Memory Flashcards
first evidence of cortical localization of memory…used electrical stimulation to map sensory/motor/language in surgery for epilepsy (*experiential/hallucinations when temporal lobe stimulated*)
Penfield
Milner did surgery on H.M and removed this to stop uncontrollable seizures….lost ability to form new long-term memories and short to long term conversion
bilateral medial temporal lobes
this memory is easy to form and easy to forget
declarative
this memory requires repetition/practice over long periods of time…less likely to be forgotten
implicit/procedural
loss of memory and/or ability to learn
amnesia
sudden onset of anterograde amnesia for short period time w/ retrograde amnesia for events since event (due to cerebral ischemia, concussion, drugs…temporary blood deprivation)
transient global amnesia
physical representation of a memory
engram
Lashley’s studies…all the cortical neurons that are activated by an external stimulus (internal representation of an object)…held in short term until activity ends, or until consolidation can occur
cell assemblies
this area is the heart for declarative memory…what makes up this area?
medial temporal lobe; hippocampus, entorhinal cortex, parahippocampal cortex
output of medial temporal lobe via this
fornix
lesion of medial temporal lobe will lose this kind of amnesia
short term (anterograde)
these parts of diencephalon is important in memory process
anterior/DM nuclei, mammillary bodies
this part of brain stores working memory
prefrontal cortex
this part of brain important for habits, motor skills, procedural memory (how to ride a bike for example)
striatum, GP, cerebellum
priming is involved with this area of brain
occipital lobe
this is damaged in Korsakoff’s syndrome
DM and mammillary bodies
acts as index of memory…pulls different parts (person, sight, smell) of memory from different memory stores
hippocampus
hippocampus necessary for this kind of memory…highly processed info stored in memory in a way that ties together all aspects that happened at time memory was stored
relational memory
where is long term memory stored?
cortex
striatum is necessary for this kind of memory
procedural
this structure is very important in remembering *places*
hippocampus
Hebb’s hypothesis claimed memory resides in these (studied Aplysia to fing out)
synaptic alterations
declarative memory is located in this part of brain
medial temporal lobe
this type of declarative memory is used for facts and general knowledge
semantic
this type of declarative memory is necessary for people, memories for autobiographical events, etc.
episodic
this NT starts a molecular cascade to sensitize a sensory axon by increasing Ca conductance…also binds GPCR (cAMP-PKA-closes K channel-depolarization/more Ca entry, increased NT release)
serotonin
Kandel’s reserach….learning occurs when this precedes Gprotein coupled activation cAMP
presynaptic Ca pulse
according to Kandel’s research…memory occurs when this occurs
K channels close and more NT released
this is basis for synaptic plasticity and motor learning in cerebellar synaptic plasticity
parallel (input adjusted for correction) and climbing fibers (error signal) on Purkinje
if these are active at same time…plasticity will occur (*marr Albus theory motor learning*)
parallel fiber synapse and climbing fiber input (on Purkinje)
these parts are considered part of episodic memory system (w/o them hippocampus receives no information)
perirhinal, parahippocampal, entorhinal cortex
Iso’s study…activation of parallel fibers alone will cause this small response..result of postsynaptic response to glutamate release by parallel fibers
long term depression
this receptor is implicated in long term depression…when only parallel fibers act on Purkinje (Ito’s study)
AMPA glutamate receptor
these can complelely block long term depression
Ca chelators
these 3 things must occur simultaneously for long term depression to occur
increase Ca (due to climbing fiber input), increase Na (due to AMPA receptor), PKC activation (due to metabotropic glutamate receptor)
learning occurs (as result of cerebellar LTD) when this occurs
Ca and Na increase and PKC activated
this occurs when AMPA channels are internalized and postsynaptic currents are depressed
memory
mammalian systems use these receptors for plasticity
glutamate
this must occur at synapses for them to be active at same time postsynaptic CA1 neuron is strongly depolarized…*in long term potentitation*
spatial and temporal summation EPSPs
these two must coincide for long term potentiation to occur
stimulation Schaffer collaterals and postsynaptic depolarization
this enhances memory longterm…binds DNA…more protein synthesis = more second messenger activation and more receptors inserted on membrane
CREB
LTP is accompanied by an increase in this
glutamate release
LTP and LTD in hippocampus rely on these receptors
NMDA
important kinase for long term memory…exposure of catalytic component necessary
CaMKII
