Abstract：
: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.
journal_name
Nat Neuroscijournal_title
Nature neuroscienceauthors
Li H,Penzo MA,Taniguchi H,Kopec CD,Huang ZJ,Li Bdoi
10.1038/nn.3322subject
Has Abstractpub_date
2013-03-01 00:00:00pages
332-9issue
3eissn
1097-6256issn
1546-1726pii
nn.3322journal_volume
16pub_type
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