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GABA 和 GABA(B)受体表达的变化与正中神经切断后大鼠楔状核神经病变有关。

Changes in GABA and GABA(B) receptor expressions are involved in neuropathy in the rat cuneate nucleus following median nerve transection.

机构信息

Department of Anatomy and Cell Biology, College of Medicine, National Taiwan University, Taipei 10018, Taiwan, Republic of China.

出版信息

Synapse. 2012 Jun;66(6):561-72. doi: 10.1002/syn.21539. Epub 2012 Feb 15.

Abstract

This study examined the relationship between changes in GABA transmission and behavioral abnormalities after median nerve transection. Following unilateral median nerve transection, the percentage of GABA-like immunoreactive neurons in the cuneate nucleus and that of GABA(B) receptor-like immunoreactive neurons in the dorsal root ganglion in the injured side decreased and reached a nadir at 4 weeks after median nerve transection. Four weeks after bilateral median nerve transection and intraperitoneal application with saline, baclofen (2 mg kg⁻¹), or phaclofen (2 mg kg⁻¹) before unilateral electrical stimulation of the injured median nerve, we investigated the level of neuropeptide Y release and c-Fos expression in the stimulated side of the cuneate nucleus. The neuropeptide Y release level and the number of c-Fos-like immunoreactive neurons in the baclofen group were significantly attenuated, whereas those in the phaclofen group had increased compared to the saline group. These findings indicate that median nerve transection reduces GABA transmission, promoting injury-induced neuropeptide Y release and consequently evoking c-Fos expression in cuneate nucleus neurons. Furthermore, this study used the CatWalk method to assess behavioral abnormalities in rats following median nerve transection. These abnormalities were reversed by baclofen treatment. Overall, the results suggest that baclofen treatment block neuropeptide Y release, subsequently lessening c-Fos expression in cuneate neurons and consequently attenuating neuropathic signal transmission to the thalamus.

摘要

本研究探讨了正中神经切断后 GABA 传递变化与行为异常的关系。正中神经切断后,患侧楔束核中 GABA 样免疫反应神经元的百分比和背根神经节中 GABA(B)受体样免疫反应神经元的百分比下降,并在正中神经切断后 4 周达到最低点。在双侧正中神经切断后 4 周,腹腔内应用生理盐水、巴氯芬(2mg/kg)或 phaclofen(2mg/kg),然后对受伤的正中神经进行单侧电刺激,我们研究了刺激侧楔束核中神经肽 Y 释放和 c-Fos 表达的水平。巴氯芬组的神经肽 Y 释放水平和 c-Fos 样免疫反应神经元的数量明显减弱,而 phaclofen 组则比生理盐水组增加。这些发现表明,正中神经切断会降低 GABA 传递,促进损伤诱导的神经肽 Y 释放,从而引起楔束核神经元的 c-Fos 表达。此外,本研究还使用 CatWalk 方法评估了正中神经切断后大鼠的行为异常。这些异常通过巴氯芬治疗得到逆转。总的来说,结果表明巴氯芬治疗可阻断神经肽 Y 的释放,从而减少楔束神经元中的 c-Fos 表达,进而减轻神经病理性信号向丘脑的传递。

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