Ogawa N, Kajita S, Sato M, Mori A
Folia Psychiatr Neurol Jpn. 1985;39(3):309-12. doi: 10.1111/j.1440-1819.1985.tb02007.x.
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.
为了研究癫痫发作与促甲状腺激素释放激素（TRH）神经系统之间的关系，通过戊四氮（PTZ）诱导的癫痫发作和杏仁核（AM）点燃来测定免疫反应性TRH（IR-TRH）和TRH受体结合活性。PTZ注射后40秒和150秒时，隔区的IR-TRH显著增加。PTZ注射后40秒和150秒时，海马体以及丘脑/中脑的IR-TRH浓度也显著增加。然而，在PTZ诱导的癫痫发作前、发作期间或发作后，未观察到TRH受体结合有显著变化。此外，在AM点燃惊厥48小时后，纹状体TRH受体出现持久变化，边缘结构中的IR-TRH短暂增加。TRH及其类似物（DN-1417）剂量依赖性地抑制PTZ诱导的全身性癫痫发作。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可能是大脑中的一种抗癫痫物质。
