Experience-dependent modification of a central amygdala fear circuit

By Haohong Li, Mario A. Penzo, H. Taniguchi, Charles D. Kopec, Z. J. Huang, Bo Li. 2013

446 citations recorded by the source corpus.

The amygdala is essential for fear learning and expression. The central amygdala (CeA), once viewed as a passive relay between the amygdala complex and downstream fear effectors, has emerged as an active participant in fear conditioning. However, the mechanism by which CeA contributes to the learning and expression of fear is unclear. We found that fear conditioning in mice induced robust plasticity of excitatory synapses onto inhibitory neurons in the lateral subdivision of the CeA (CeL). This experience-dependent plasticity was cell specific, bidirectional and expressed presynaptically by inputs from the lateral amygdala. In particular, preventing synaptic potentiation onto somatostatin-positive neurons impaired fear memory formation. Furthermore, activation of these neurons was necessary for fear memory recall and was sufficient to drive fear responses. Our findings support a model in which fear conditioning–induced synaptic modifications in CeL favor the activation of somatostatin-positive neurons, which inhibit CeL output, thereby disinhibiting the medial subdivision of CeA and releasing fear expression.

Subfields: Cellular and Molecular Neuroscience, Cognitive Neuroscience, Social Psychology

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Citations in the corpus

A temporal shift in the circuits mediating retrieval of fear memory (2015, background): “01, SAL: n= 6; MUS: n= 7) (f) In separate animals, PL inactivation also impaired fear retrieval at 7 d after conditioning (F(1,14)= 13.”
AMYGDALA MICROCIRCUITS CONTROLLING LEARNED FEAR (2014, background): “Second, selective ICM lesions (Likhtik et al., 2008) as well as pharmacological inhibition of BLA inputs to ICM cells by neuropeptide S (Jü ngling et al., 2008) interfere with extinction.”