癫痫发作与大鼠脑促甲状腺素释放激素(TRH)神经系统的关系。

N Ogawa, S Kajita, M Sato, A Mori
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引用次数: 4

摘要

为了研究癫痫发作与促甲状腺素释放激素(TRH)神经系统的关系,采用戊四唑(PTZ)诱导癫痫发作和杏仁核(AM)点燃法测定免疫反应性TRH (IR-TRH)和TRH受体结合活性。注射PTZ后40、150秒,中隔IR-TRH明显升高。注射PTZ后40秒和150秒,海马和丘脑/中脑的IR-TRH浓度也显著增加。然而,在ptz诱导的癫痫发作之前,期间或之后,TRH受体结合未观察到显著变化。此外,AM点燃惊厥48小时后,纹状体TRH受体的持续变化以及边缘结构的短暂IR-TRH增加。TRH及其类似物(DN-1417)对ptz诱导的全身性癫痫发作具有剂量依赖性。这些发现表明TRH神经系统参与癫痫发作机制,并提示内源性TRH可能是大脑中的抗癫痫物质。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Seizures and thyrotropin-releasing hormone (TRH) neural system in the rat brain.

In order to study the relationship between seizures and the thyrotropin-releasing hormone (TRH) neural system, immunoreactive TRH (IR-TRH) and TRH receptor binding activity were determined by pentylenetetrazol (PTZ)-induced seizures and amygdaloid (AM) kindling. IR-TRH markedly increased in the septum 40 and 150 seconds after the PTZ injection. A significant increase in the IR-TRH concentrations was also noted in the hippocampus and thalamus/midbrain 40 and 150 seconds after the PTZ injection, respectively. However, no significant changes were observed in the TRH receptor binding before, during or after the PTZ-induced seizures. In addition, a lasting change in the striatal TRH receptors after AM kindling as well as a transient IR-TRH increase in the limbic structures were seen 48 hours after Am-kindled convulsions. TRH and its analog (DN-1417) inhibited PTZ-induced generalized seizures dose-dependently. These findings indicate the involvement of the TRH neural system in seizure mechanisms, and suggest that endogenous TRH may be an antiepileptic substance in the brain.

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