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。