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首页> 外文期刊>The European Journal of Neuroscience >Nicotine recruits a local glutamatergic circuit to excite septohippocampal GABAergic neurons.
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Nicotine recruits a local glutamatergic circuit to excite septohippocampal GABAergic neurons.

机译：尼古丁募集局部谷氨酸能回路来激发海马GABA能神经元。

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摘要

Tonic impulse flow in the septohippocampal GABAergic pathway is essential for normal cognitive functioning and is sustained, in part, by acetylcholine (ACh) that is released locally via axon collaterals of septohippocampal cholinergic neurons. Septohippocampal cholinergic neurons degenerate in Alzheimer's disease and other neurodegenerative disorders. While the importance of the muscarinic effects of ACh on septohippocampal GABAergic neurons is well recognized, the nicotinic effects of ACh remain unstudied despite the reported benefits of nicotine on cognitive functioning. In the present study, using electrophysiological recordings in a rat brain slice preparation, rapid applications of nicotine excited 90% of retrogradely labelled septohippocampal GABA-type neurons with an EC50 of 17 microm and increased the frequency of spontaneously occurring, impulse-dependent fast GABAergic and glutamatergic synaptic currents via the alpha4beta2-nicotinic receptor. Interestingly, tetrodotoxin blocked all effects of nicotine on septohippocampal GABAergic type neurons, suggesting involvement of indirect mechanisms. We demonstrate that the effects of nicotine on septohippocampal GABA-type neurons involve recruitment of a novel, local glutamatergic circuitry as (i). Group I metabotropic glutamatergic receptor antagonists reduced the effects of nicotine; (ii). the number of nicotine responsive neurons was significantly reduced in recordings from slices that had been trimmed so as to reduce the number of glutamate-containing neurons within the slice preparation; (iii). in light and ultrastructural double immunocytochemical labelling studies vesicular glutamate 2 transporter immunoreactive terminals made synaptic contacts with parvalbumin-immunoreactive septohippocampal GABAergic neurons. The discovery of a local glutamatergic circuit within the septum may provide another avenue for restoring septohippocampal GABAergic functions in neurodegenerative disorders associated with a loss of septohippocampal cholinergic neurons.
机译：在海马GABA能通路中的冲动冲动对于正常的认知功能是必不可少的，并且部分由乙酰胆碱（ACh）维持，该乙酰胆碱通过海马胆碱能神经元的轴突侧支在局部释放。隔海马胆碱能神经元在阿尔茨海默氏病和其他神经退行性疾病中退化。尽管人们公认ACh的毒蕈碱作用对海马GABA能级神经元的重要性，但尽管已报道了尼古丁对认知功能的益处，但仍未研究ACh的烟碱作用。在本研究中，使用大鼠脑切片制备过程中的电生理记录，快速应用尼古丁可以激发90％的逆行标记海马GABA型神经元，其EC50为17微米，并增加了自发发生，依赖冲动的快速GABA能和通过alpha4beta2-烟碱受体的谷氨酸能突触电流。有趣的是，河豚毒素阻断了尼古丁对海马GABA能型神经元的所有作用，提示其间接机制的参与。我们证明尼古丁对隔海马GABA型神经元的影响涉及（i）募集新型的局部谷氨酸能电路。第一组代谢型谷氨酸能受体拮抗剂降低了尼古丁的作用。 （ii）。修剪过的切片的记录中尼古丁反应神经元的数量大大减少，从而减少了切片制品中含谷氨酸的神经元的数量; （iii）。在光和超微结构双重免疫细胞化学标记研究中，囊泡谷氨酸2转运蛋白的免疫反应性末端与小白蛋白免疫反应性海马GABA能神经元发生突触接触。在隔膜内发现局部谷氨酸能循环可能为恢复与海马胆碱能神经元丧失相关的神经退行性疾病中的海马GABA能功能提供另一条途径。

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