Stress enables synaptic depression in CA1 synapses by acute and chronic morphine: Possible mechanisms for corticosterone on opiate addiction
文献类型：期刊论文
| 作者 | Yang Y1,2; Zheng XG3; Cao JX4; Sui N[*]3; Xu L[*]1,2; Wang YF4; Cao J1,2; Dong ZF1,2 |
| 刊名 | JOURNAL OF NEUROSCIENCE
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| 出版日期 | 2004 |
| 卷号 | 24期号:10页码:2412-2420 |
| 关键词 | hippocampus long-term depression associative learning stress morphine-seeking opiate addiction |
| 通讯作者 | suin@psych.ac.cn ; lxu@vip.163.com |
| 英文摘要 | The hippocampus, being sensitive to stress and glucocorticoids, plays significant roles in certain types of learning and memory. Therefore, the hippocampus is probably involved in the increasing drug use, drug seeking, and relapse caused by stress. We have studied the effect of stress with morphine on synaptic plasticity in the CA1 region of the hippocampus in vivo and on a delayed-escape paradigm of the Morris water maze. Our results reveal that acute stress enables long-term depression (LTD) induction by low-frequency stimulation (LFS) but acute morphine causes synaptic potentiation. Remarkably, exposure to an acute stressor reverses the effect of morphine from synaptic potentiation ( similar to 20%) to synaptic depression ( similar to 40%), precluding further LTD induction by LFS. The synaptic depression caused by stress with morphine is blocked either by the glucocorticoid receptor antagonist RU38486 or by the NMDA-receptor antagonist D-APV. Chronic morphine attenuates the ability of acute morphine to cause synaptic potentiation, and stress to enable LTD induction, but not the ability of stress in tandem with morphine to cause synaptic depression. Furthermore, corticosterone with morphine during the initial phase of drug use promotes later delayed-escape behavior, as indicated by the morphine-reinforced longer latencies to escape, leading to persistent morphine-seeking after withdrawal. These results suggest that hippocampal synaptic plasticity may play a significant role in the effects of stress or glucocorticoids on opiate addiction. |
| 收录类别 | SCI |
| 资助信息 | Chinese Academy of Sciences Grants KSCX2-SW-204-02(N.S.)and KSCX-SW-204-04 (L.X.), National Natural Science Foundation of China Grants 30170324 and 30230130 (N.S.) and 39870280, 39925011, and 39930080 (L.X.), and National Basic Research Program Grants 2003CB515404 (N.S.) and G1999054000(L.X.). |
| 语种 | 英语 |
| 源URL | [http://159.226.149.26:8080/handle/152453/10900]  |
| 专题 | 昆明动物研究所_学习记忆的分子神经机制 |
| 作者单位 | 1.Chinese Acad Sci, Kunming Inst Zool, Lab Learning & Memory, Kunming 650223, Peoples R China 2.Chinese Acad Sci, Grad Sch, Beijing 100039, Peoples R China 3.Chinese Acad Sci, Inst Psychol, Key Lab Mental Hlth, Beijing 100101, Peoples R China 4.Chinese Acad Sci, Kunming Inst Zool, Lab Behav & Brain, Kunming 650223, Peoples R China |
| 推荐引用方式 GB/T 7714 | Yang Y,Zheng XG,Cao JX,et al. Stress enables synaptic depression in CA1 synapses by acute and chronic morphine: Possible mechanisms for corticosterone on opiate addiction[J]. JOURNAL OF NEUROSCIENCE,2004,24(10):2412-2420. |
| APA | Yang Y.,Zheng XG.,Cao JX.,Sui N[*].,Xu L[*].,...&Dong ZF.(2004).Stress enables synaptic depression in CA1 synapses by acute and chronic morphine: Possible mechanisms for corticosterone on opiate addiction.JOURNAL OF NEUROSCIENCE,24(10),2412-2420. |
| MLA | Yang Y,et al."Stress enables synaptic depression in CA1 synapses by acute and chronic morphine: Possible mechanisms for corticosterone on opiate addiction".JOURNAL OF NEUROSCIENCE 24.10(2004):2412-2420. |
入库方式： OAI收割
来源：昆明动物研究所
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