Synaptic mechanisms regulating cardiovascular afferent inputs to solitary tract nucleus.
Synaptic mechanisms regulating cardiovascular afferent inputs to solitary tract nucleus.
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调节心血管传入孤束核的突触机制。
DOI：
10.1152/ajpheart.1990.259.3.h653
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
R. Felder
中科院分区：
文献类型：
--
作者：
S. Mifflin;R. Felder
这篇简短的综述总结了最近有关中枢神经系统内心血管传入输入的初始处理的电生理学研究。这项工作表明，压力感受器传入纤维的终止部位，孤束核（nTS），不仅仅是一个简单的中继站。来自不同反射区的传入输入之间的相互作用以及取决于传入输入时间的相互作用可以以抑制或促进的方式影响 nTS 神经元的输出，从而确定这些神经元传递到随后参与心血管调节的中枢核的信号。此外，来自更多头侧结构（例如下丘脑防御区和臂旁核）的下行输入可以进一步改变 nTS 神经元对压力感受器输入的反应性。有证据表明，在反射通路的早期阶段存在调节压力反射增益的神经基质。
This brief review summarizes recent electrophysiological studies concerning the initial processing of cardiovascular afferent inputs within the central nervous system. This work has shown that the site of termination of baroreceptor afferent fibers, the nucleus of the tractus solitarius (nTS), is much more than a simple relay station. Interactions between afferent inputs from different reflexogenic areas and interactions that depend on the timing of the afferent inputs can influence the output of nTS neurons in either an inhibitory or facilitatory manner and thereby determine the signal that these neurons relay to subsequent central nuclei involved in cardiovascular regulation. In addition, descending inputs from more rostral structures (e.g., the hypothalamic defense area and the parabrachial nucleus) can further alter the responsiveness of nTS neurons to baroreceptor inputs. The evidence suggests that the neural substrates exist for a modulation of baroreflex gain at an early stage in the reflex pathway.