Palkovits M, Young W S, Kovács K, Tóth Z, Makara G B
Laboratory of Neuromorphology, Semmelweis University Medical School, Budapest, Hungary.
Neuroscience. 1998 Jul;85(1):135-47. doi: 10.1016/s0306-4522(97)00621-0.
Corticotropin-releasing hormone messenger RNA expression in the amygdala of rats after adrenalectomy and bilateral lesions of the hypothalamic paraventricular nucleus was examined by in situ hybridization histochemistry. Corticotropin-releasing hormone messenger RNA-containing cells are abundant in the intermediate subdivision of the central amygdaloid nucleus. Some corticotropin-releasing hormone-labeled cells are scattered in other subdivisions of the central nucleus and throughout the anterior amygdaloid area. Five days after bilateral adrenalectomy, the number of corticotropin-releasing hormone messenger RNA-containing cells was reduced both in the central nucleus and the anterior area of the amygdala. This reduction was prevented by corticosterone replacement and contrasts sharply with the known rise of corticotropin-releasing hormone messenger RNA in the paraventricular nucleus after adrenalectomy. Corticotropin-releasing hormone messenger RNA expression in the amygdala was up-regulated in rats with six-week bilateral lesions of the paraventricular nucleus. This elevation in corticotropin-releasing hormone messenger RNA was not influenced by adrenalectomy or corticosterone, and it did not correlate with plasma levels of adrenocorticotrophic hormone or corticosterone. The possible direct innervation of the amygdala by the paraventricular nucleus is supported by the demonstration of labeled axons from the paraventricular nucleus to the amygdala after injection of an anterograde tracer, Phaseolus vulgaris leucoagglutinin, into the paraventricular nucleus. Labeled fibers take two courses: through the lateral hypothalamus ventral amygdalofugal path and through the stria terminalis. Data presented here suggest that the paraventricular nucleus-amygdala connection is likely to be inhibitory to corticotropin-releasing hormone neurons in the central amygdala. These neurons may participate in behavioral responses to stress effected through brainstem autonomic centers rather than directly through the hypothalamo-pituitary adrenal axis.
采用原位杂交组织化学方法，研究了肾上腺切除及下丘脑室旁核双侧损伤后大鼠杏仁核中促肾上腺皮质激素释放激素信使核糖核酸（CRH mRNA）的表达。含CRH mRNA的细胞在杏仁中央核中间亚区丰富。一些CRH标记的细胞散在于中央核的其他亚区以及整个杏仁前区。双侧肾上腺切除5天后，杏仁核中央核和前区含CRH mRNA的细胞数量减少。皮质酮替代可防止这种减少，这与肾上腺切除后室旁核中已知的CRH mRNA升高形成鲜明对比。在室旁核双侧损伤6周的大鼠中，杏仁核中CRH mRNA表达上调。这种CRH mRNA的升高不受肾上腺切除或皮质酮的影响，且与促肾上腺皮质激素或皮质酮的血浆水平无关。将顺行示踪剂菜豆凝集素注入室旁核后，显示从室旁核到杏仁核的标记轴突，支持了室旁核对杏仁核可能存在直接神经支配。标记纤维有两条路径：通过下丘脑外侧腹侧杏仁核传出通路和终纹床核。此处呈现的数据表明，室旁核 - 杏仁核连接可能对杏仁中央核中的CRH神经元具有抑制作用。这些神经元可能参与通过脑干自主神经中枢而非直接通过下丘脑 - 垂体 - 肾上腺轴实现的应激行为反应。
