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


ABSTRACT: 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.

SUBMITTER: Jing L 

PROVIDER: S-EPMC4598857 | biostudies-literature | 2015 Oct

REPOSITORIES: biostudies-literature

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

Jing Liang L   Duan Ting-Ting TT   Tian Meng M   Yuan Qiang Q   Tan Ji-Wei JW   Zhu Yong-Yong YY   Ding Ze-Yang ZY   Cao Jun J   Yang Yue-Xiong YX   Zhang Xia X   Mao Rong-Rong RR   Richter-Levin Gal G   Zhou Qi-Xin QX   Xu Lin L  

Scientific reports 20151009


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  ...[more]

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