期刊
JOURNAL OF NEURAL TRANSMISSION
卷 120, 期 11, 页码 1525-1531出版社
SPRINGER WIEN
DOI: 10.1007/s00702-013-1032-y
关键词
Protein synthesis; mTOR; Amygdala; Inhibitory avoidance; Memory strengthening; Fear memory
资金
- National Council for Scientific and Technological Development (CNPq) [303703/2009-1, 484185/2012-8]
- National Institute for Translational Medicine (INCT-TM)
- HCPA institutional research fund (FIPE/HCPA)
- Coordination for the Improvement of Higher Education Personnel (CAPES)
Fear memory retrieval can lead to either reconsolidation (accompanied or not by strengthening of the memory trace) or extinction. Here, we show that non-reinforced retrieval of inhibitory avoidance (IA) conditioning can induce memory strengthening assessed in a subsequent retention test trial. Infusion of the protein synthesis inhibitor cycloheximide or the mTOR inhibitor rapamycin into the rat basolateral complex of the amygdala (BLA) after a reactivation (retrieval) session impaired retrieval-induced strengthening. Intra-BLA infusion of the mRNA synthesis inhibitor 5,6-dichloro-1-beta-d-ribofuranosylbenzimidazole (DRB) after retrieval had no effect. These findings provide the first evidence suggesting that non-reinforced IA retrieval can lead to memory strengthening through a mechanism dependent on protein synthesis and mTOR activity in the BLA.
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