Chp 15 - The fate of retrieved memories Flashcards
what are the two perspectives on retrieval functions of memory
destabilization function - retrieving a memory returned it into a vulnerable state for disruption
integrative function - role of the brain is to access the new content and integrate it with previously acquired information. it results in a new engram that contains both retrieved and new information
Lewis fear-conditioning experiment to study vulnerability of a reactivated memory
CS and US together, 24 hours past, one group was reactivated (only CS) and had either a ECS (shock) or no ECS then 24 hours and test.
Other group CS and US together, 24 hours, no reactivation, ECS or no ECS, 24 hours, then test.
Results show that reactivation and ECS had the worse results/response time. - because memory reactivated making it vulnerable, then shock disrupted the memory
Memories can be present in what two states
short term memory, active
long term memory, inactive
how does a novel experience activate short and long term memory and how does retrieval cues
novel (new) experience - connects to short term active memory - into long term inactive state
retrieval cues (retrieving a memory) - connects to long term memory inactive state - then activates short term (vulnerable state) - then back into long term
CS and US paired together, 24 hours, Reactivation, either anisomycin or vehicle given, given either short term or long term test –> 4 hours, CS (short term memory test), 24 hours (long term memory test). Results?
anisomycin is protein synthesis inhibitor.
anisomycin disrupted long term retention of the reactivated fear memory but no effect on short term retention which is true because protein synthesis not needed for short term
when retrieval cues activate consolidated but inactive memory… what occurs to long term memory is protein synthesis occurs or is prevented
when retrieved the trace becomes vulnerable and initiates protein synthesis and the memory is reconsolidated, long term memory still conserved.
when retrieved and protein synthesis is prevented, the memory trace and long term memory is weakened when it returns back to inactive state
What is the key events that destabilize the synaptic basis of a memory trace
glutamate releases - calcium levels increase by NMDA and VGCCs - either scaffolding proteins are ubiquitinated which leads to proteasome degrades scaffolding proteins - or CaMKII activated - either proteasome phosphorylated or proteasome translocated from dendritic shaft to spine - proteasome degrades scaffolding protein - AMPA receptor endocytosis and depotentiation of the synapse
(spine gets smaller and removes AMPA receptors)
In the events of destabilization of the synaptic basis of a memory trace, if NMDA and VGCCs are inhibited prior to reactivation, what occurs
the trace will not be destabilized and therefore not be able to be altered/ vulnerable
In the events of destabilization of the synaptic basis of a memory trace, if proteasome is inhibited, what occurs
it is inhibited by anisomycin and it will not affect the reactivated memory because new protein is not needed to restabilize the trace
context shock - 24 hours - drug or vehicle - context only (reactivation) - 24 hours - long term memory test, results of different drugs?
just anisomycin before reactivation produces amnesia (reduced freezing)
(anisomycin and Blac) inhibiting proteasome with Blac prevented destabilization therefore never got destabilized so anisomycin had no chance to reduce protein synthesis
prediction error hypothesis of destabilization
when there is a mismatch between the information retrieved from memory and current experience this prediction error will trigger the UPS system to destabilize the trace
experiment for prediction errors destabilizing the engram
CS - 30 seconds - then US (all trained this way 10 times) then 24 hours passes - one group still CS 30 seconds US, other group CS - 10 SECONDS - US.
done with both vehicle and anisomycin
prediction error is made in the group that had 10 seconds between.
the group 2 that had anisomycin produced less freezing because it destabilized the engram and become vulnerable to change and therefore showed less fear
To add additional learning information to already existing memory must cause the trace to be
destabilized because inhibiting proteasome activity by infusing Blac prevents additional learning added because it is not destabilized
What is the time window for altering a reactivated memory
within a 15min-1hour time limit in which the trace remains destabilized
How does CNQX effect memory retrieval
it is an AMPA receptor antagonist which prevents the expression of the response when the engram is reactivated (effects reactivation)
