Experience-dependent modification of a central amygdala fear circuit

被引:352
作者
Li, Haohong [1 ]
Penzo, Mario A. [1 ]
Taniguchi, Hiroki [1 ]
Kopec, Charles D. [2 ]
Huang, Z. Josh [1 ]
Li, Bo [1 ]
机构
[1] Cold Spring Harbor Lab, Cold Spring Harbor, NY 11724 USA
[2] Princeton Univ, Dept Mol Biol, Princeton, NJ 08544 USA
基金
美国国家卫生研究院;
关键词
LONG-TERM POTENTIATION; CENTRAL NUCLEUS; RECEPTOR TRAFFICKING; CONDITIONED FEAR; PROJECTIONS; NEURONS; RAT; EXPRESSION; COMPLEX; CONNECTIONS;
D O I
10.1038/nn.3322
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
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.
引用
收藏
页码:332 / 339
页数:8
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