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食欲素通过激活非选择性阳离子通道增强巨细胞网状核的放电活动。

Orexin enhances firing activities in the gigantocellular reticular nucleus through the activation of non-selective cationic conductance.

机构信息

Department of Physiology, Army Medical University, Chongqing 400038, PR China.

Department of Physiology, Army Medical University, Chongqing 400038, PR China.

出版信息

Neurosci Lett. 2020 Aug 10;733:135088. doi: 10.1016/j.neulet.2020.135088. Epub 2020 May 25.

DOI:10.1016/j.neulet.2020.135088
PMID:32464262
Abstract

Orexin/hypocretin has been implicated in central motor control. The gigantocellular reticular nucleus (Gi), a key element of the brainstem motor inhibitory system, also receives orexinergic innervations. However, the modulations of orexin on the neuronal activities and the underlying cellular mechanisms in Gi neurons remain unknown. Here, through whole-cell patch-clamp recordings, we first observed that orexin increased the firing frequency in Gi neurons. Interestingly, a postsynaptic depolarization elicited by orexin was observed in the presence of tetrodotoxin, without altering the input resistance of Gi neurons at around -60 mV. Moreover, through comparing the current-frequency curves constructed by identical current injections from equal membrane potentials, we found that orexin also increased the repetitive firing ability of Gi neurons. This action appeared to be caused by the shortening of inter-spike intervals, without altering the waveform of individual action potentials. We finally revealed that activation of the non-selective cationic conductance contributed to the orexin-elicited excitation in Gi neurons. Together, these results suggest that orexin may facilitate Gi-mediated motor functions through enhancing the neuronal activities of Gi neurons.

摘要

食欲素/下丘脑分泌素参与了中枢运动控制。巨细胞网状核(Gi)是脑干运动抑制系统的关键要素,也接收食欲素能神经支配。然而,食欲素对 Gi 神经元的神经元活动的调制及其潜在的细胞机制仍不清楚。在这里,我们通过全细胞膜片钳记录首先观察到,食欲素增加了 Gi 神经元的放电频率。有趣的是,在存在河豚毒素的情况下,观察到由食欲素引起的突触后去极化,而不会改变 Gi 神经元在约-60 mV 的输入电阻。此外,通过比较从相同膜电位进行相同电流注入构建的电流-频率曲线,我们发现食欲素也增加了 Gi 神经元的重复放电能力。这种作用似乎是由于峰间间隔的缩短引起的,而不会改变单个动作电位的波形。我们最后揭示,非选择性阳离子电导的激活导致 Gi 神经元中食欲素引起的兴奋。总之,这些结果表明,食欲素可能通过增强 Gi 神经元的神经元活动来促进 Gi 介导的运动功能。

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