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

doi:10.1038/srep15000

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 journal › Article › peer-review

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.

Original language	English
Article number	15000
Journal	Scientific Reports
Volume	5
DOIs	https://doi.org/10.1038/srep15000
State	Published - 9 Oct 2015

Bibliographical note

Funding Information:
This work was supported by 973 program from the Ministry of Science and Technology of China (2013CB835103 to L.X.), the National Science Foundation of China (31100775 and 31371141 to Q-X.Z.), Strategic Priority Research Program of the Chinese Academy of Sciences (XDB02020002), External Cooperation Program of BIC of Chinese Academy of Sciences (GJHZ1549) and Science and Technology Program of Yunnan Province (2013GA003).

Publisher Copyright:
© 2015 Macmillan Publishers Limited.

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@article{247973bd1ed445ebb5195c2bb46f1e5d,

title = "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.",

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

note = "Funding Information: This work was supported by 973 program from the Ministry of Science and Technology of China (2013CB835103 to L.X.), the National Science Foundation of China (31100775 and 31371141 to Q-X.Z.), Strategic Priority Research Program of the Chinese Academy of Sciences (XDB02020002), External Cooperation Program of BIC of Chinese Academy of Sciences (GJHZ1549) and Science and Technology Program of Yunnan Province (2013GA003). Publisher Copyright: {\textcopyright} 2015 Macmillan Publishers Limited.",

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doi = "10.1038/srep15000",

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AU - Jing, Liang

AU - Duan, Ting Ting

AU - Tian, Meng

AU - Yuan, Qiang

AU - Tan, Ji Wei

AU - Zhu, Yong Yong

AU - Ding, Ze Yang

AU - Cao, Jun

AU - Yang, Yue Xiong

AU - Zhang, Xia

AU - Mao, Rong Rong

AU - Richter-Levin, Gal

AU - Zhou, Qi Xin

AU - Xu, Lin

N1 - Funding Information: This work was supported by 973 program from the Ministry of Science and Technology of China (2013CB835103 to L.X.), the National Science Foundation of China (31100775 and 31371141 to Q-X.Z.), Strategic Priority Research Program of the Chinese Academy of Sciences (XDB02020002), External Cooperation Program of BIC of Chinese Academy of Sciences (GJHZ1549) and Science and Technology Program of Yunnan Province (2013GA003). Publisher Copyright: © 2015 Macmillan Publishers Limited.

PY - 2015/10/9

Y1 - 2015/10/9

N2 - 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.

AB - 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.

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

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