Hippocampal synaptic transmission enhanced by low concentrations of nicotine
Hippocampal synaptic transmission enhanced by low concentrations of nicotine
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DOI：
10.1038/383713a0
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发表时间：
1996-10-24
期刊：
影响因子：
64.8
通讯作者：
Dani, JA
中科院分区：
文献类型：
--
作者：
Gray, R;Rajan, AS;Dani, JA
从烟草中获得的尼古丁可以改善各种任务的学习和记忆，并与唤醒，注意力，快速信息处理，工作记忆和长期记忆有关，这些记忆可以在戒烟后引起渴望（1，2）。这些作用的一个可能靶点是海马，海马是一个学习和记忆中心，具有丰富的胆碱能神经支配和密集的烟碱乙酰胆碱受体（nAChR）表达（3-6）。在阿尔茨海默氏痴呆症期间，nAChR较少，海马的胆碱能输入退化（7）。然而，没有证据表明海马体中nAChR介导的快速突触传递，并且其作用尚不清楚（8，9）。已知尼古丁作用于小鸡缰核内的突触前nAChR，以增强海马能传递（10）;在此，我们报告了在海马体中的类似机制。单苔藓纤维突触前末梢细胞内Ca 2+的测量表明，含有α 7亚基的nAChRs可以介导足以诱导囊泡神经递质释放的Ca 2+内流。我们认为烟草中的尼古丁通过增强突触传递来影响认知。相反，降低的传输效率可以解释与阿尔茨海默病期间胆碱能神经支配丧失相关的缺陷。
NICOTINE obtained from tobacco can improve learning and memory on various tasks and has been linked to arousal, attention, rapid information processing, working memory, and longterm memories that can cause craving years after someone has stopped smoking(1,2). One likely target for these effects is the hippocampus, a centre for learning and memory that has rich cholinergic innervation and dense nicotinic acetylcholine receptor (nAChR) expression(3-6). During Alzheimer's dementia there are fewer nAChRs and the cholinergic inputs to the hippocampus degenerate(7). However, there is no evidence for fast synaptic transmission mediated by nAChRs in the hippocampus, and their role is not understood(8,9). Nicotine is known to act on presynaptic nAChRs within the habenula of chick to enhance glutamatergic transmission(10); here we report that a similar mechanism operates in the hippocampus. Measurements of intracellular Ca2+ in single mossy-fibre presynaptic terminals indicate that nAChRs containing the alpha 7 subunit can mediate a Ca2+ influx that is sufficient to induce vesicular neurotransmitter release. We propose that nicotine from tobacco influences cognition by enhancing synaptic transmission. Conversely, a decreased efficacy of transmission may account for the deficits associated with the loss of cholinergic innervation during Alzheimer's disease.