Stress evoked by opiate withdrawal facilitates hippocampal LTP in vivo
Stress evoked by opiate withdrawal facilitates hippocampal LTP in vivo
复制标题
阿片戒断引起的压力促进体内海马 LTP
DOI：
10.1002/hipo.20234
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发表时间：
2006-01-01
期刊：
影响因子：
3.5
通讯作者：
Xu, Lin
中科院分区：
文献类型：
--
作者：
Dong, Zhifang;Zhong, Weixia;Xu, Lin
应激对海马长时程增强（LTP）有影响，但阿片戒断引起的应激是否有同样的影响尚不清楚。本研究报告阿片类药物戒断4天不影响基础突触传递，但导致麻醉大鼠海马CA1区LTP显著增加。平台应激升高使停药18小时的大鼠出现较大的LTP，但糖皮质激素受体拮抗剂RU38486（每天两次，持续3天）阻止了停药4天的大LTP。此外，停药4 d可增强nmdar介导的EPSC，含nr2a介导的EPSC增加，含nr2b介导的EPSC减少。这些结果表明，在4天的阿片戒断期间，NMDAR和糖皮质激素受体功能的适应性变化可能使应激促进海马LTP，可能有助于阿片戒断经验依赖性海马功能的修改。(c) 2006 Wiley-Liss, Inc。
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 Elevated-platform stress enabled a large LTP in rats withdrawn for only 18 h, but the glucocorticoid receptor antagonist RU38486 (twice per day for 3 days) prevented the large LTP on 4 days withdrawal.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. (c) 2006 Wiley-Liss, Inc.