Muscarine activates the sodium-calcium exchanger via M receptors in basal forebrain neurons.

Muscarine activates the sodium-calcium exchanger via M receptors in basal forebrain neurons.
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毒蕈碱通过基底前脑神经元中的 M 受体激活钠钙交换器。

DOI:
10.1111/j.1460-9568.2006.05118.x
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发表时间:
2006
期刊:
The European journal of neuroscience
影响因子:
--
通讯作者:
Alreja,Meenakshi
Alreja,Meenakshi
中科院分区:
--
文献类型:
--
作者:
Xu,Changqing;Wu,Min;Morozova,Elena;Alreja,Meenakshi

文献摘要

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内侧隔/Broca对角带(MSDB)的神经元投射到海马。MSDB中的毒蕈碱胆碱能机制是海马功能的有效调节剂;隔内东莨菪碱破坏和隔内卡巴胆碱促进海马依赖性学习和记忆任务以及相关的海马θ节律。在早期的工作中,我们证明,在MSDB,隔海马GABA能神经元,但不是胆碱能神经元是毒蕈碱操纵的主要目标和毒蕈碱激活隔海马GABA能神经元直接介导的M3受体。在本研究中,我们研究了毒蕈碱在这些神经元中兴奋作用的离子机制。在大鼠脑切片中使用全细胞膜片钳记录技术,我们证明了M3受体介导的MSDB神经元的毒蕈碱激活依赖于外部Na+,并且也被浴用Ni 2+和KB-R7943以及用Li+替代外部Na+所减少,这表明Na+-Ca 2+交换剂的主要参与。我们的结论是,M3受体介导的毒蕈碱激活MSDB隔海马GABA型神经元,这是重要的认知功能,是通过激活Na+-Ca 2+交换介导的。
Neurons of the medial septum/diagonal band of Broca (MSDB) project to the hippocampus. Muscarinic cholinergic mechanisms within the MSDB are potent modulators of hippocampal functions; intraseptal scopolamine disrupts and intraseptal carbachol facilitates hippocampus‐dependent learning and memory tasks, and the associated hippocampal theta rhythm. In earlier work, we demonstrated that, within the MSDB, the septohippocampal GABAergic but not cholinergic neurons are the primary target of muscarinic manipulations and that muscarinic activation of septohippocampal GABAergic neurons is mediated directly via M3receptors. In the present study, we examined the ionic mechanism(s) underlying the excitatory actions of muscarine in these neurons. Using whole‐cell patch‐clamp recording techniques in rat brain slices, we demonstrated that M3receptor‐mediated muscarinic activation of MSDB neurons is dependent on external Na+and is also reduced by bath‐applied Ni2+and KB‐R7943 as well as by replacing external Na+with Li+, suggesting a primary involvement of the Na+–Ca2+exchanger. We conclude that the M3receptor‐mediated muscarinic activation of MSDB septohippocampal GABA‐type neurons, that is important for cognitive functioning, is mediated via activation of the Na+–Ca2+exchanger.