Abstract

Memory is supported by a specific collection of neurons distributed in broad brain areas, an engram. Despite recent advances in identifying an engram, how the engram is created during memory formation remains elusive. To explore the relation between a specific pattern of input activity and memory allocation, here we target a sparse subset of neurons in the auditory cortex and thalamus. The synaptic inputs from these neurons to the lateral amygdala (LA) are not potentiated by fear conditioning. Using an optogenetic priming stimulus, we manipulate these synapses to be potentiated by the learning. In this condition, fear memory is preferentially encoded in the manipulated cell ensembles. This change, however, is abolished with optical long-term depression (LTD) delivered shortly after training. Conversely, delivering optical long-term potentiation (LTP) alone shortly after fear conditioning is sufficient to induce the preferential memory encoding. These results suggest a synaptic plasticity-dependent competition rule underlying memory formation.

Highlights

  • We examined whether the lateral amygdala (LA) synapses can be primed for long-term potentiation (LTP) induction by using a pattern of optogenetic synaptic stimulation that precedes fear conditioning control (FC) (Fig. 1a)

  • We reported that a pattern of 10-Hz optogenetic stimulation of both thalamic and cortical inputs in the LA simultaneously can drive an associative fear memory formation as a CS when paired with a footshock[20]

  • We found that LTP was elicited 5 min and 1 d after training in mice received the opto-stimulation before FC

Read more

Summary

Introduction

Delivering optical long-term potentiation (LTP) alone shortly after fear conditioning is sufficient to induce the preferential memory encoding These results suggest a synaptic plasticitydependent competition rule underlying memory formation. Many studies over the past decade have identified ensembles of neurons and synapses where engram is thought to be localized These cells and synapses are the brain sites where learning-dependent physical changes occur and are crucial for the later retrieval of memory[2,3,4,5,6,7]. We show changes in cell ensembles that participate in encoding a fear memory in a competitive manner by a specific pattern of optogenetic synaptic stimulations related to synaptic plasticity delivered right before or after learning

Objectives
Methods
Results
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call