Inactivation of α7 ACh receptors and activation of non-α7 ACh receptors both contribute to long term potentiation induction in the hippocampal CA1 region
Inactivation of α7 ACh receptors and activation of non-α7 ACh receptors both contribute to long term potentiation induction in the hippocampal CA1 region
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DOI：
10.1016/s0304-3940(00)01076-4
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发表时间：
2000-06-02
影响因子：
2.5
通讯作者：
Sumikawa, K
中科院分区：
文献类型：
--
作者：
Fujii, S;Ji, ZX;Sumikawa, K
急性和慢性尼古丁暴露不同地促进了海马CA1区长时程增强(LTP)的诱导，LTP是一种学习和记忆的突触模型。然而，尼古丁的这些效应背后的机制尚不清楚。在本研究中，烟碱型乙酰胆碱受体(NAChR)激动剂和α7 nAChR拮抗剂均促进幼年大鼠海马CA1区LTP的诱导。此外，慢性尼古丁治疗降低了LTP的诱导阈值，而急性应用尼古丁激动剂而不是α7拮抗剂，进一步促进了慢性尼古丁治疗的海马LTP的诱导。这些结果表明，不仅非α7 nAChRs的激活和α7 nAChRs的失活都有助于LTP的诱导，而且慢性尼古丁介导的LTP诱导是由于慢性尼古丁诱导的α7 nAChRs的脱敏，(C)2000 Elsevier Science爱尔兰有限公司。保留所有权利。
Acute and chronic nicotine exposure differentially facilitate the induction of long-term potentiation (LTP), a synaptic model of learning and memory, in the hippocampal CA1 region. The mechanisms underlying these effects of nicotine, however, are unknown. In the present study, both nicotinic acetylcholine receptor (nAChR) agonists and an alpha 7 nAChR antagonist facilitated the induction LTP in the hippocampal CA1 region of naive rat. Furthermore, chronic nicotine treatment lowered the threshold for induction of LTP, and acute application of nicotinic agonists, but not an alpha 7 antagonist, further facilitated LTP induction in the chronic-nicotine-treated hippocampus. These results suggest not only that both activation of non-alpha 7 nAChRs and inactivation of alpha 7 nAChRs contribute to LTP induction, but also that chronic-nicotine-mediated facilitation of LTP induction is due to chronic-nicotine-induced desensitization of alpha 7 nAChRs, (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.