Jamieson S M, Harris M C
Department of Physiology, Medical School, Birmingham, U.K.
Neuroscience. 1989;32(1):227-34. doi: 10.1016/0306-4522(89)90121-8.
Stimulation of carotid body chemoreceptors activates putative vasopressin neurons in the supraoptic nucleus, an effect which has been abolished by lesions in the caudal ventrolateral medulla. Stimulation within the A1 catecholamine cell group in the ventrolateral medulla also activates supraoptic neurons and releases vasopressin. Therefore the A1 catecholamine neurons may be the means by which carotid body chemoreceptors influence the supraoptic nucleus and other parts of the forebrain. To test this possibility the influence of carotid body chemoreceptors on the discharge of rostrally-projecting neurons in the A1 region of the caudal ventrolateral medulla has been assessed in rats anaesthetized with a mixture of urethane and sodium pentobarbitone. Tests were performed on 131 neurons, 23 of which were antidromically invaded following electrical stimulation within the supraoptic nucleus, the medial forebrain bundle or the ventral noradrenergic bundle. The positions of all antidromically invaded neurons were marked with dye and in six animals subsequent fluorescence histochemistry showed that the blue spots were in the proximity of one or more catecholamine-containing cell bodies in the ventrolateral medulla. The recorded neurons were therefore presumed to be part of the A1 group of catecholamine-containing neurons. All neurons located were tested for their responses to specific stimulation of ipsilateral carotid body chemoreceptors and also to general baroreflex activation. Not one of the antidromically invaded neurons was affected by chemoreceptor stimulation and only one was activated by baroreflex activation. Of the non-antidromically invaded neurons, seven were activated and 13 were depressed following chemoreceptor stimulation but in many cases the latency to onset was very long.(ABSTRACT TRUNCATED AT 250 WORDS)
刺激颈动脉体化学感受器可激活视上核中假定的血管加压素神经元,尾侧腹外侧延髓受损后该效应消失。刺激延髓腹外侧的A1儿茶酚胺细胞群也可激活视上核神经元并释放血管加压素。因此,A1儿茶酚胺神经元可能是颈动脉体化学感受器影响视上核及前脑其他部分的途径。为验证这一可能性,在用乌拉坦和戊巴比妥钠混合麻醉的大鼠中,评估了颈动脉体化学感受器对尾侧腹外侧延髓A1区向头端投射神经元放电的影响。对131个神经元进行了测试,其中23个在视上核、内侧前脑束或腹侧去甲肾上腺素能束内电刺激后被逆向激活。所有逆向激活神经元的位置都用染料标记,在6只动物中,随后的荧光组织化学显示蓝色斑点靠近延髓腹外侧一个或多个含儿茶酚胺细胞体。因此,记录的神经元被认为是含儿茶酚胺神经元A1组的一部分。对所有定位的神经元测试了它们对同侧颈动脉体化学感受器特异性刺激的反应以及对一般压力反射激活的反应。逆向激活的神经元中没有一个受到化学感受器刺激的影响,只有一个因压力反射激活而被激活。在未逆向激活的神经元中,7个在化学感受器刺激后被激活,13个被抑制,但在许多情况下,开始反应的潜伏期很长。(摘要截断于250字)