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Related Experiment Video

Updated: Jun 5, 2026

Investigating the Neural Mechanisms of Aware and Unaware Fear Memory with fMRI

Investigating the Neural Mechanisms of Aware and Unaware Fear Memory with fMRI

Published on: October 6, 2011

Central amygdala activity during fear conditioning.

Sevil Duvarci¹, Daniela Popa, Denis Paré

¹Center for Molecular and Behavioral Neuroscience, Rutgers, The State University of New Jersey, Newark, New Jersey 07102, USA.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience

|January 7, 2011

Summary

This summary is machine-generated.

The central amygdala (CeM) drives conditioned fear. Fear conditioning increases CeM activity, while extinction reduces it. The central lateral amygdala (CeL) shows plasticity, suggesting a model for fear memory.

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Last Updated: Jun 5, 2026

Investigating the Neural Mechanisms of Aware and Unaware Fear Memory with fMRI

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Published on: October 6, 2011

Ex Vivo Optogenetic Dissection of Fear Circuits in Brain Slices

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Published on: April 5, 2016

Trace Fear Conditioning in Mice

Trace Fear Conditioning in Mice

Published on: March 20, 2014

Area of Science:

Neuroscience
Behavioral Neuroscience

Background:

The central amygdala (Ce), specifically the medial division (CeM), is crucial for conditioned fear responses.
The precise role of CeM in controlling conditioned fear remains unclear.

Purpose of the Study:

To investigate the neural mechanisms underlying CeM control of conditioned fear using in vivo recordings in rats.
To elucidate the functional changes in CeM and CeL neuronal activity during fear conditioning, recall, and extinction.

Main Methods:

Unit recordings were performed in rats during fear conditioning, recall tests, and extinction training.
Analysis focused on conditioned stimulus (CS)-evoked firing rates in CeM and CeL neurons.
Cell-by-cell analysis identified excitatory (CeL(+)) and inhibitory (CeL(-)) CS-evoked responses in CeL.

Main Results:

Fear conditioning increased CS responsiveness in most CeM neurons, which persisted during recall and diminished with extinction.
CeL neurons showed heterogeneous CS-evoked responses, with an increase in inhibitory (CeL(-)) cells from conditioning to recall.
Extinction training reduced CS-evoked activity in both CeM and CeL.

Conclusions:

Conditioned freezing is associated with enhanced CeM responses to the CS.
Fear conditioning induces overnight synaptic plasticity in inhibitory inputs to CeL, leading to increased CeL(-) activity.
A model is proposed where fear conditioning potentiates an inhibitory input to CeL, disinhibiting CeM neurons and driving fear responses.