AT_1受体在脑胆碱能刺激引起的孤束核TH-IR变化中的作用

THE ROLE OF AT_1 RECEPTOR IN THE CHANGES OF TH-IR IN NUCLEUS OF SOLITARY TRACT INDUCED BY BRAIN CHOLINERGIC STIMULATION

本工作选用清醒SD雄性大鼠,利用免疫组织化学方法,观察大鼠侧脑室注射胆碱能激动剂氨甲酰胆碱后孤束核内儿茶酚胺能神经元活性的变化以及阻断脑AT1受体对上述变化的影响。免疫组织化学结果显示:侧脑室注射氨甲酰胆碱(.5μg)后40 min,孤束核内酪氨酸羟化酶(TH)免疫反应阳性神经元数目明显增多(P<0.05),免疫染色强度明显增强(P<0.05)。losartan(20μg)预处理后孤束核内TH免疫反应活性明显下降(P<0.05)。上述结果提示,侧脑室注射胆碱能激动剂氨甲酰胆碱对孤束核内儿茶酚胺能神经元具有兴奋作用,阻断脑血管紧张素能AT1受体可部分抑制氨甲酰胆碱在孤束核诱导的上述变化。

In the present study, we investigated the thyrosine hydroxylase immunoreactivity (TH-IR) in nucleus of solitary tract (Sol) after intracerebroventricular (i. c. v. ) injection of carbachol in conscious SD rats by immunohistochemistry. Meanwhile the effect of blocking AT1 receptor was also observed. The results demonstrated that both mean gray and number of TH IR positive neurons were markedly increased in nucleus of solitary tract after 40 minutes of i. c. v. injection of carbachol (0. 5 μg) . The enhancement was significantly reduced by i. c. v. injection of losartan. The above results suggest that i. c. v. injection of cholinergic agonist carbachol can enhance the activity of adrenergic neurons in nucleus of solitary tract. The blockade of AT1 receptor may down-regulate the above action induced by carbachol in nucleus of solitary tract.