Despair-associated memory requires a slow-onset CA1 long-term potentiation with unique underlying mechanisms

Liang Jing, Ting Ting Duan, Meng Tian, Qiang Yuan, Ji Wei Tan, Yong Yong Zhu, Ze Yang Ding, Jun Cao, Yue Xiong Yang, Xia Zhang, Rong Rong Mao, Gal Richter-Levin, Qi Xin Zhou, Lin Xu

Research output: Contribution to journalArticlepeer-review


The emotion of despair that occurs with uncontrollable stressful event is probably retained by memory, termed despair-associated memory, although little is known about the underlying mechanisms. Here, we report that forced swimming (FS) with no hope to escape, but not hopefully escapable swimming (ES), enhances hippocampal α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR)-dependent GluA1 Ser831 phosphorylation (S831-P), induces a slow-onset CA1 long-term potentiation (LTP) in freely moving rats and leads to increased test immobility 24-h later. Before FS application of the antagonists to block S831-P or N-methyl-D-aspartic acid receptor (NMDAR) or glucocorticoid receptor (GR) disrupts LTP and reduces test immobility, to levels similar to those of the ES group. Because these mechanisms are specifically linked with the hopeless of escape from FS, we suggest that despair-associated memory occurs with an endogenous CA1 LTP that is intriguingly mediated by a unique combination of rapid S831-P with NMDAR and GR activation to shape subsequent behavioral despair.

Original languageEnglish
Article number15000
JournalScientific Reports
StatePublished - 9 Oct 2015

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© 2015 Macmillan Publishers Limited.

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