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Sci Rep. 2015 Oct 9;5:15000. doi: 10.1038/srep15000.

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

Jing L1,2, Duan TT1,3, Tian M1,2, Yuan Q1,2, Tan JW1,2, Zhu YY1,3, Ding ZY1,4, Cao J1,2, Yang YX1,2, Zhang X5, Mao RR1,2, Richter-Levin G6,7, Zhou QX1,2, Xu L1,2,8,9.

Author information

Key Laboratory of Animal Models and Human Disease Mechanisms, and KIZ/CUHK Joint Laboratory of Bioresources and Molecular Research in Common Disease, and Laboratory of Learning and Memory, Kunming Institute of Zoology, the Chinese Academy of Sciences, Kunming 650223, China.
University of the Chinese Academy of Sciences, Beijing 100049, China.
School of Life Sciences, University of Science and Technology of China, Hefei 230027, China.
School of Life Sciences, Anhui University, Hefei 230601, China.
Institute of Mental Health Research and Departments of Psychiatry and Cellular &Molecular Medicine, University of Ottawa, 1145 Carling Ave, Ottawa, Ontario, K1Z 7K4, Canada.
Sagol Department of Neurobiology and Department of Psychology, University of Haifa, Haifa, Israel.
The Institute for the Study of Affective Neuroscience, University of Haifa, Haifa, Israel.
CAS Center for Excellence in Brain Science, 320 Yue Yang Road, Shanghai, 200031, China.
Mental Health Institute, the Second Xiangya Hospital of Central South University, Changsha 410011, China.


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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