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Stress evoked by opiate withdrawal facilitates hippocampal LTP in vivo
Author(s) -
Dong Zhifang,
Zhong Weixia,
Tian Meng,
Han Huili,
Cao Jun,
Xu Tianle,
Luo Jianhong,
Xu Lin
Publication year - 2006
Publication title -
hippocampus
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.767
H-Index - 155
eISSN - 1098-1063
pISSN - 1050-9631
DOI - 10.1002/hipo.20234
Subject(s) - long term potentiation , hippocampal formation , nmda receptor , opiate , glucocorticoid receptor , neuroscience , antagonist , kindling , hippocampus , excitatory postsynaptic potential , glucocorticoid , chemistry , glutamate receptor , neurotransmission , psychology , endocrinology , medicine , receptor , stimulation , inhibitory postsynaptic potential
Stress impairs hippocampal long‐term potentiation (LTP), but it is unknown whether the stress evoked by opiate withdrawal has the same effect. Here the authors report that opiate withdrawal for 4 days does not influence basal synaptic transmission, but results in a greatly increased LTP in hippocampal CA1 area in anesthetized rats. Elevated‐platform stress enabled a large LTP in rats withdrawn for only 18 h, but the glucocorticoid receptor antagonist RU38486 (twice per day for 3 days) prevented the large LTP on 4 days withdrawal. Moreover, 4 days withdrawal enhanced the NMDAR‐mediated EPSCs, in which the NR2A‐containing NMDAR‐mediated EPSC was increased but the NR2B‐containing NMDAR‐mediated EPSC was decreased. These results suggest that adaptive changes of the NMDAR and glucocorticoid receptor functions during 4 days of opiate withdrawal may enable stress to facilitate hippocampal LTP, potentially contributing to the opiate withdrawal experience‐dependent modifications of hippocampal functions. © 2006 Wiley‐Liss, Inc.