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BIO SCI N156 Lecture 18: Memory Reconsolidating; Memory System Interactions
BIO SCI N156 Lecture 18: Memory Reconsolidating; Memory System Interactions
Reactivated Memory
Can disrupt reactivated memory by ECS
When memory trace was reactivated, and then given ECS, the memory for the CS-shock experience was disrupted
Once the consolidation window closes, ECS has no influence on the memory
ECS had no effect on memory when it was presented in the absence of shock
Active trace theory
Retrieval cues tap back into the LTM trace
Brings LTM into STM active state that needs to be re-consolidated
Makes the memory labile again
Memories in active state are vulnerable, those in inactive state are not
Reconsolidation theory
Nader's finding
Rats conditioned to auditory cue-shock pairing
Following reactivation of fear, inject anisomycin (protein synthesis inhibitor) or vehicle into lateral nucleus of amygdala
Rats given either a STM or LTM test
Anisomycin disrupted long-term retention of reactivated fear memory, but no effect on short-term retention of memory
Blocked the re-consolidation of the reactivated memory
Normal state:
Retrieval cue recalls LTM trace, activates many of same synapse that were active during learning
Retrieval initiates protein synthesis, memory trace reconsolidated
Will be stable when it returns to inactive state
If protein synthesis is prevented, the memory trace will be weakened or lost when it return to inactive state
Assessing the theory
Only the reactivated memory trace needs to be re-consolidated
Rats acquire two fear memories (CS1 and CS2)
Give drug or vehicle just prior to reactivation
Only the reactivated memory (CS1) was disrupted by drug U0126, which interferes with consolidation (blocks activation of MAP kinase, which is necessary for LTP)
STM was not disrupted
LTM of the CS1 was disrupted by U0126
The latent cue (CS2) was not disrupted by the drug
How reactivation destabilizes the trace
Role of UPS: protein get ubiquitinated, targeted for degradation
With glutamate release during retrieval, many of same synapses active during learning get reactivated
Scaffold proteins degraded by UPS, CaMKII activated
AMPA receptor endocytosis
If preteosomes are inhibited, reconsolidating is uncessary
Inhibiting proteasome function blocks anisomycin's effect
if protein is not degraded, there is not need for new protein
Standard model of consolidation vs. reconsolidation
Conventional view: Retrieval of experience
Learning, storage, retrieval
Each time the memory is activated, a trace of the original experience is retrieved
Reconsolidating view: Retrieval of last storage
Learning, storage, retrieval, storage, retrieval
Memories are susceptible to change each time they are retrieved
The memory activated during retrieval is the version stored during the last retrieval
Perhaps reconsolidation allows memory traces to be updated to incorporate new information
Memory formation and retrieval are not necessarily independent processes
Information encoding and memory retrieval likely interact dynamically
The information from past traces may influence short/working memory
Trace Destabilization and Updating
Reactived trace can be strengthened
Inject PKA activator BZN-cAMP into BLA following reactivation trials of tone-shock conditioning
Increased rat's fear response to a CS paired with shock
Injecting PKA activator without reactivating the fear memory had no effect
Injecting PKA inhibitor with reactivated impaired subsequent memory retrieval
Disrupting memory reconsolidation
Newly formed memory may undergo reconsolidation, but older ones may not
Anisomycin disrupted memory reconsolidation of recently formed memories, but not older ones
Poor performance at test: memory storage or retrieval failure?
Memories can be disrupted for two reasons
Storage failue
Amnesia is permanent
Retrieval failure
Amnesia is temporary
Disrupting even can interfere with storage of memory trace or it can interfere with processes involved in retrieval
Evidence for memory retrieval [not storage] failure
Transient memory retrieval failure after inactivation of amygdala after memory reactivation
Infuse TTX into amygdala either after initial training or after retrieval test
Infusion after training: consolidation loss is permanent
Infusion after first retrieval test: consolidation loss is temporary; memory was profoundly inaccessible for a few days after the TTX injection
Disrupting memory reconsolidation
Potential therapy for preventing drug relapse
Blocking zif268 protein expression (with AS ODNs) disrupted consolidation of light-drug memory associations
Rats given zif268 AS ODN did not show the return to high lever drug-seeking behavior, while controls did
Zif268 is a TF IEG implicated in synaptic plasticity
Train rats to associate drug with a light cue
Rats given extinction training
BLA infused with the zif268 AS ODN or scrambled AS ODN at start of extinction training