期刊
NATURE NEUROSCIENCE
卷 16, 期 10, 页码 1436-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nn.3491
关键词
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资金
- National Research Foundation of Korea
- Ministry of Education, Science and Technology [2011-0018209, 2011-0019226]
- Original Technology Research Program for Brain Science through the National Research Foundation of Korea
- Korean World Class Institute program
- Brain Korea 21 Research Fellowships from the Korean Ministry of Education
- National Research Foundation of Korea [2011-0019226] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Fear renewal, a widely pursued model of post-traumatic stress disorder and phobias, refers to the context-specific relapse of conditioned fear after extinction. However, its molecular mechanisms are largely unknown. We found that renewal-inducing stimuli, generally believed to be insufficient to induce synaptic plasticity, enhanced excitatory synaptic strength, activity of synaptic GluA2-lacking AMPA receptors and Ser831 phosphorylation of synaptic surface GluA1 in the lateral nucleus of the amygdala (LAn) of fear-extinguished rats. Consistently, the induction threshold for LAn synaptic potentiation was considerably lowered after extinction, and renewal occluded this low-threshold potentiation. The low-threshold potentiation (a potential cellular substrate for renewal), but not long-term potentiation, was attenuated by dialysis into LAn neurons of a GluA1-derived peptide that competes with Ser831-phosphorylated GluA1. Microinjections of the same peptide into the LAn attenuated fear renewal, but not fear learning. Our findings suggest that GluA1 phosphorylation constitutes a promising target for clinical treatment of aberrant fear-related disorders.
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