Smith D W, Day T A
Department of Physiology and Pharmacology, University of Queensland, Australia.
Neuroscience. 1994 Feb;58(4):765-75. doi: 10.1016/0306-4522(94)90453-7.
Noxious somatic stimuli elicit vasopressin secretion, an effect thought to result from activation of a facilitatory input from A1 catecholamine cells of the medulla oblongata. To better characterize the A1 cell response and effects on other neuroendocrine A1 projection targets, particularly within the paraventricular nucleus, we have now mapped c-fos expression in neurochemically identified catecholamine and neurosecretory cells following a noxious somatic stimulus. Unilateral hind paw pinch significantly increased c-fos expression in contralateral A1 cells whereas other brainstem catecholamine cell groups were unaffected. Expression of c-fos was also increased in the supraoptic nucleus, this effect being more pronounced for vasopressin than oxytocin neurosecretory cells and, as with A1 cells, primarily on the side contralateral to the stimulated paw. In contrast, the increase in the paraventricular nucleus was greater in oxytocin rather than in vasopressin cells. Additionally there was a significant rise in c-fos expression in medial parvocellular paraventricular nucleus cells of noxiously stimulated animals. Notably, the majority of tuberoinfundibular corticotropin-releasing factor cells are located in this medial parvocellular zone. These results are consistent with and expand on those previously reported from electrophysiological and anatomical studies. The finding of differing neurosecretory cell responses between supraoptic and paraventricular nuclei has interesting implications with regard to the afferent control of neurosecretory cell activity. For example, the substantially greater activation of supraoptic versus paraventricular nucleus vasopressin cells, despite being innervated by the same medullary noradrenergic cell group, raises the possibility of a differential input or differences in responsiveness. Furthermore, the activation of paraventricular nucleus parvocellular cells is consistent with suggestions that the A1 cell group provides an excitatory input to this population.
伤害性躯体刺激会引发血管加压素分泌，一般认为这种效应是由延髓A1儿茶酚胺细胞的易化性输入激活所致。为了更好地描述A1细胞的反应及其对其他神经内分泌A1投射靶点的影响，尤其是在室旁核内的影响，我们现在绘制了伤害性躯体刺激后神经化学鉴定的儿茶酚胺和神经分泌细胞中的c-fos表达图谱。单侧后爪挤压显著增加了对侧A1细胞中的c-fos表达，而其他脑干儿茶酚胺细胞群未受影响。视上核中的c-fos表达也增加了，这种效应在血管加压素神经分泌细胞中比催产素神经分泌细胞中更明显，并且与A1细胞一样，主要在受刺激爪的对侧。相比之下，室旁核中催产素细胞的增加幅度大于血管加压素细胞。此外，在受到伤害性刺激的动物的室旁核小细胞内侧核细胞中，c-fos表达显著升高。值得注意的是，大多数结节漏斗促肾上腺皮质激素释放因子细胞位于这个室旁核小细胞内侧区。这些结果与先前电生理和解剖学研究报告的结果一致并有所扩展。视上核和室旁核之间神经分泌细胞反应不同的发现，对于神经分泌细胞活动的传入控制具有有趣的意义。例如，尽管视上核和室旁核的血管加压素细胞由同一延髓去甲肾上腺素能细胞群支配，但视上核血管加压素细胞的激活程度明显高于室旁核，这增加了存在差异输入或反应性差异的可能性。此外，室旁核小细胞的激活与A1细胞群向该群体提供兴奋性输入的观点一致。
