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不同谷氨酸受体在模拟微重力后大鼠红核神经元谷氨酸诱发兴奋介导中的作用。

The role of different glutamate receptors in the mediation of glutamate-evoked excitation of red nucleus neurons after simulated microgravity in rat.

作者信息

Yang Jian-Chang, Fan Xiao-Li, Song Xin-Ai, Li Qiang

机构信息

Department of Physiology and Pathophysiology, Xi'an Jiaotong University School of Medicine, Xi'an Yanta Street W 76#, Xi'an, Shaanxi 710061, China.

出版信息

Neurosci Lett. 2008 Dec 31;448(3):255-9. doi: 10.1016/j.neulet.2008.10.044. Epub 2008 Oct 17.

DOI:10.1016/j.neulet.2008.10.044
PMID:18950683
Abstract

The present study investigates changes in red nucleus (RN) neuronal activity and the role of glutamate receptors (GluRs) after simulated microgravity (tail-suspension) in the rat using single-unit recording and microinjection. The results showed that tail-suspension for 3, 7, and 14 days could induce a significant decrease in spontaneous firing rate of RN neurons in a time-dependent manner. Unilateral microinjection of glutamate into the RN significantly increased the firing rate of RN neurons, but the increased firing rate was significantly reduced following tail-suspension time. Microinjection of the NMDA receptor antagonist MK-801 or the non-NMDA receptor antagonist DNQX into the RN blocked this excitatory effect induced by glutamate. However, microinjection of the metabotropic glutamate receptor (mGluR) antagonist (+/-)-MCPG into the RN had no effect. These results suggest that simulated microgravity can reduce excitability of RN neurons following a functional impairment of glutamate receptors. NMDA and non-NMDA receptors, but not mGluRs, are involved in the mediation of glutamate-evoked excitation of RN neurons. The decrease in excitability of RN neurons may be involved in simulated microgravity-induced muscle atrophy.

摘要

本研究采用单单位记录和微注射技术,研究了模拟微重力(尾部悬吊)后大鼠红核(RN)神经元活动的变化以及谷氨酸受体(GluRs)的作用。结果表明,尾部悬吊3天、7天和14天可导致RN神经元的自发放电率随时间呈显著下降。向RN单侧微注射谷氨酸可显著提高RN神经元的放电率,但随着尾部悬吊时间的延长,增加的放电率显著降低。向RN微注射NMDA受体拮抗剂MK-801或非NMDA受体拮抗剂DNQX可阻断谷氨酸诱导的这种兴奋作用。然而,向RN微注射代谢型谷氨酸受体(mGluR)拮抗剂(+/-)-MCPG则没有效果。这些结果表明,模拟微重力可在谷氨酸受体功能受损后降低RN神经元的兴奋性。NMDA和非NMDA受体而非mGluRs参与介导谷氨酸诱发的RN神经元兴奋。RN神经元兴奋性的降低可能与模拟微重力诱导的肌肉萎缩有关。

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