Chan R K, Jarvina E V, Sawchenko P E
Laboratory of Neuronal Structure and Function, The Salk Institute for Biological Studies, La Jolla, CA 92037, USA.
Neuroscience. 2000;101(1):165-78. doi: 10.1016/s0306-4522(00)00332-8.
Intravenous administration of phenylephrine provokes a pattern of cellular activation in the nucleus of the solitary tract that resembles the central distributions of primary baroreceptor afferents supplied by the carotid sinus and aortic depressor nerves. Transganglionic transport and denervation methods were used in an experimental setting to test the dependence of phenylephrine-induced Fos immunoreactivity on the integrity of buffer nerve afferents, and to identify the subregions of the nucleus of the solitary tract supplied by each. Cholera toxin B-horseradish peroxidase injections into either or both nerves revealed terminal labeling concentrated in, but not restricted to, the dorsal commissural part of the nucleus of the solitary tract at the level of the apex of calamus scriptorius, and extending into the dorsal subnucleus at the level of the area postrema. Preferential ramifications of carotid sinus and aortic depressor nerve afferents at the levels of the commissural part of the nucleus and the area postrema, respectively, were reflected in the extent to which labeled fibers comingled with neurons exhibiting phenylephrine-induced Fos in dual labeling experiments. Complete sinoaortic denervation reduced by 90% the number of neurons exhibiting drug-induced Fos expression. Selective carotid and aortic sinus denervations effected partial reductions manifest preferentially in the caudal and rostral foci of the distribution, respectively. Reduced activational responses at the level of the area postrema of aortic sinus-denervated rats were accompanied by a reduction in cellular nicotinamide adenine dinucleotide phosphate-diaphorase activity in this region. Animals killed 30 days after complete sinoaortic denervation displayed no evidence of recovery of phenylephrine-induced Fos, while the strength and distribution of the response in rats that received selective carotid sinus denervation were indistinguishable from those seen in controls. These findings (i) support the dependence of phenylephrine-induced Fos expression on the integrity of carotid sinus and aortic depressor nerve afferents, (ii) provide anatomical and functional evidence that the two buffer nerves distribute differentially within the nucleus of the solitary tract, and (iii) implicate central reorganization as a likely basis for functional recovery of baroreflex mechanisms following partial sinoaortic denervation.
静脉注射去氧肾上腺素会在孤束核中引发一种细胞激活模式，这种模式类似于由颈动脉窦和主动脉减压神经提供的初级压力感受器传入纤维的中枢分布。在实验环境中使用跨神经节运输和去神经支配方法，以测试去氧肾上腺素诱导的Fos免疫反应性对缓冲神经传入纤维完整性的依赖性，并确定每条神经所供应的孤束核亚区域。向一条或两条神经注射霍乱毒素B-辣根过氧化物酶，显示终末标记集中在但不限于书写叶尖水平的孤束核背连合部，并延伸到最后区水平的背侧亚核。颈动脉窦和主动脉减压神经传入纤维分别在孤束核连合部和最后区水平的优先分支，反映在双标实验中标记纤维与表现出去氧肾上腺素诱导的Fos的神经元混合的程度上。完全的窦主动脉去神经支配使表现出药物诱导的Fos表达的神经元数量减少了90%。选择性颈动脉和主动脉窦去神经支配分别导致部分减少，分别优先在分布的尾侧和头侧焦点出现。主动脉窦去神经支配大鼠最后区水平的激活反应降低，同时该区域细胞烟酰胺腺嘌呤二核苷酸磷酸-黄递酶活性降低。完全窦主动脉去神经支配30天后处死的动物没有显示出去氧肾上腺素诱导的Fos恢复的证据，而接受选择性颈动脉窦去神经支配的大鼠的反应强度和分布与对照组无明显差异。这些发现：（i）支持去氧肾上腺素诱导的Fos表达对颈动脉窦和主动脉减压神经传入纤维完整性的依赖性；（ii）提供了解剖学和功能证据，表明两条缓冲神经在孤束核内的分布不同；（iii）暗示中枢重组可能是部分窦主动脉去神经支配后压力反射机制功能恢复的基础。
