Chemoreceptor and baroreceptor responses of A1 area neurons projecting to supraoptic nucleus.

Chemoreceptor and baroreceptor responses of A1 area neurons projecting to supraoptic nucleus.
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A1 区神经元投射到视上核的化学感受器和压力感受器反应。

DOI:
10.1152/ajpregu.1992.263.2.r310
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发表时间:
1992
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
W. Blessing
W. Blessing
中科院分区:
--
文献类型:
--
作者:
Y. W. Li;Z. Gieroba;W. Blessing

文献摘要

被引文献

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在乌拉坦麻醉兔的A1区,对127个神经元进行了细胞外记录,这些神经元是由视上核的逆行激活所鉴定的。中位轴突传导速度为0.7m/S,中位放电频率为3.9个/S,其中94个神经元的放电频率随动脉压升高而降低。降低动脉压可使50个受试神经元的放电频率增加。在70个被压力感受器激活抑制的神经元中,40个被高二氧化碳低氧兴奋,25个被高二氧化碳抑制。在高碳酸血症兴奋的23个神经元中,所有神经元都受到缺氧的刺激,但只有2个神经元受到高碳酸血症的影响。在被高碳酸血症抑制的16个神经元中,15个被低氧抑制,1个被高碳酸血症抑制。在低氧兴奋的14个神经元中,有13个是通过颈总动脉注射氰化钠兴奋的。在被缺氧抑制的5个神经元中,有4个被氰化钠抑制。我们的结果提供了电生理学证据,从A1区投射到视上核的神经元在压力感受器卸载时增加其放电频率,而在压力感受器激活时降低其放电频率。这些神经元可能构成中枢通路的一部分,调节血管加压素的分泌以应对出血。很高比例的神经元也接受外周化学感受器输入,这些A1细胞也可能是中枢通路的一部分,通过化学感受器刺激改变加压素的分泌。
Extracellular recordings were made from 127 neurons, identified by antidromic activation from the supraoptic nucleus, in the A1 area of urethan-anesthetized rabbits. The median axonal conduction velocity was 0.7 m/s, and the median discharge rate was 3.9 spikes/s. Raising arterial pressure decreased the discharge rate in 94 of 101 neurons tested. Lowering arterial pressure increased the discharge rate in 50 of 64 neurons tested. Of 70 neurons inhibited by baroreceptor activation, 40 were excited and 25 inhibited by hypercapnic hypoxia. Of 23 neurons excited by hypercapnic hypoxia, all were excited by hypoxia but only 2 were affected by hypercapnia. Of 16 neurons inhibited by hypercapnic hypoxia, 15 were inhibited by hypoxia and 1 was inhibited by hypercapnia. Of 14 neurons excited by hypoxia, 13 were excited by injection of sodium cyanide into the common carotid artery. Of five neurons inhibited by hypoxia, four were inhibited by sodium cyanide. Our results provide electrophysiological evidence that neurons projecting from the A1 area to the supraoptic nucleus increase their discharge rate in response to baroreceptor unloading and decrease their discharge rate in response to baroreceptor activation. These neurons may form part of the central pathway mediating secretion of vasopressin in response to hemorrhage. A high proportion of the neurons also receive peripheral chemoreceptor inputs, and these A1 cells may also be part of the central pathway whereby chemoreceptor stimulation modifies the secretion of vasopressin.