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正中神经损伤诱导大鼠楔状核甘氨酸受体表达减少导致 NPY 释放和 c-Fos 表达。

Decreases of glycine receptor expression induced by median nerve injury in the rat cuneate nucleus contribute to NPY release and c-Fos expression.

机构信息

Department of Anatomy and Cell Biology, College of Medicine, National Taiwan University, 1-1 Jen Ai Road, Taipei, Taiwan.

出版信息

Life Sci. 2012 Feb 13;90(7-8):278-88. doi: 10.1016/j.lfs.2011.11.014. Epub 2011 Dec 8.

Abstract

AIMS

This study aimed to investigate temporal changes in glycine and its receptor expressions in cuneate neurons after median nerve transection (MNT), and the effects of glycine on neuropeptide Y (NPY) release and c-Fos expression in the cuneate nucleus (CN).

MAIN METHODS

Immunohistochemistry methods were used to appraise changes of glycine- and GlyR-like immunoreactive (LI) neurons in the CN after MNT. The alterations in NPY and c-Fos expressions were used to assess the effects of saline, glycine or strychnine treatment. The CatWalk method was used to assess the efficiency of glycine treatment on the neuropathic signs of rats with MNT.

KEY FINDINGS

Approximately half of GlyR-LI neurons were fluorogold-labeled cuneothalamic projection neurons in the CN. Following MNT, the number of GlyR-LI neurons significantly decreased in the injured side of CN at 2 and 4 weeks, but the number of glycine-LI neurons remained unchanged. Four weeks after MNT given with electrical stimulation, strychnine significantly decreased the NPY reduction level in the stimulated side CN compared to that of the saline group. However, numbers of c-Fos-LI neurons in the glycine and strychnine groups were both significantly less than that in the saline group. But the paw print width and area in CatWalk analysis showed only a moderate recovery.

SIGNIFICANCE

We conjecture that glycine increases glycine-mediated postsynaptic inhibition of cuneate neurons, and also blocks GABAergic neurons containing GlyRs which mediate presynaptic inhibition causing temperate NPY release. Consequently, the compromise results showed a weak reduction in c-Fos expression and a slight amelioration of neuropathic behaviors.

摘要

目的

本研究旨在探讨正中神经切断(MNT)后楔状核(CN)中甘氨酸及其受体表达的时间变化,以及甘氨酸对 CN 中神经肽 Y(NPY)释放和 c-Fos 表达的影响。

主要方法

免疫组织化学方法评估 MNT 后 CN 中甘氨酸和 GlyR 样免疫反应(LI)神经元的变化。使用 NPY 和 c-Fos 表达的改变来评估盐水、甘氨酸或士的宁处理的影响。CatWalk 方法用于评估 MNT 大鼠甘氨酸治疗对神经病理性体征的效果。

主要发现

CN 中约一半的 GlyR-LI 神经元是氟金标记的楔状丘脑投射神经元。MNT 后 2 周和 4 周时,CN 损伤侧的 GlyR-LI 神经元数量显著减少,但甘氨酸-LI 神经元数量保持不变。MNT 后 4 周给予电刺激时,与生理盐水组相比,士的宁显著降低了刺激侧 CN 中 NPY 的减少水平。然而,甘氨酸和士的宁组的 c-Fos-LI 神经元数量均明显少于生理盐水组。但 CatWalk 分析中的足印宽度和面积仅显示出中度恢复。

意义

我们推测甘氨酸增加了 CN 中甘氨酸介导的突触后抑制,并且还阻断了介导 presynaptic 抑制的含有 GlyRs 的 GABA 能神经元,导致 NPY 释放适度增加。因此,结果显示 c-Fos 表达减少和神经病理性行为改善微弱。

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