The area postrema: a cardiovascular control centre at the blood-brain interface?
The area postrema: a cardiovascular control centre at the blood-brain interface?
复制标题
后区：血脑界面的心血管控制中心？
DOI：
10.1139/y91-153
复制
发表时间：
1991
影响因子：
2.1
通讯作者：
Alastair V. Ferguson
中科院分区：
文献类型：
--
作者：
Alastair V. Ferguson
最后区（AP）是大脑的室周器官之一，因此它是高度血管化的，缺乏正常的血脑屏障。解剖追踪研究表明，AP的传入投射来自室旁核、臂旁外侧核（l-PBN）、孤束核（NTS）以及迷走神经。AP神经元已被证明主要投射到l-PBN和NTS。受体定位研究已经报道了AP中许多特异性肽受体的密集聚集，包括血管紧张素II（ANG）、心钠素（ANP）和内皮素（ET）的那些。电刺激研究表明，AP神经元在低频（低于15 Hz）下的激活会导致血压和心率下降，而高频（高于20 Hz）刺激会导致血压升高。这些对血压和心率的低频影响似乎是由自主神经系统的独立成分的激活引起的。细胞外单单位记录已经确定了两个功能上独立的AP神经元群体：一个对循环ANG有反应，另一个对血压变化有明显反应。此外，AP神经元被循环ET的增加激活。从1-PBN到AP神经元的传入输入对相对小比例的AP神经元具有单独的兴奋性（AP神经元的12%）或抑制性（AP神经元的12%）作用。相比之下，初步证据表明，一个更广泛分布的兴奋性输入约70%的测试AP神经元起源于主动脉降压神经。这些研究提供了相当多的证据暗示AP作为一个重要的神经结构调节心血管系统。
The area postrema (AP) is one of the circumventricular organs of the brain and as such it is highly vascular and lacks the normal blood-brain barrier. Anatomical tracing studies have demonstrated afferent projections to AP originating from the paraventricular nucleus, lateral parabrachial nucleus (l-PBN), nucleus tractus solitarius (NTS), as well as the vagus nerve. AP neurons have been shown to project primarily to l-PBN, and NTS. Receptor localization studies have reported dense aggregations of many specific peptide receptors in AP including those for angiotensin II (ANG), atrial natriuretic peptide (ANP), and endothelin (ET). Electrical stimulation studies have shown that activation of AP neurons at low frequencies (less than 15 Hz) results in decreases in blood pressure and heart rate, while higher frequency (greater than 20 Hz) stimulation causes increases in blood pressure. These low frequency effects on blood pressure and heart rate appear to result from activation of separate components of the autonomic nervous system. Extracellular single unit recordings have identified two functionally separate populations of AP neurons: one responsive to circulating ANG and a second apparently responsive to changes in blood pressure. In addition, AP neurons are activated by increases in circulating ET. Afferent inputs to AP neurons from 1-PBN have separate excitatory (12% of AP neurons) or inhibitory (12% of AP neurons) effects on a relatively small proportion of AP neurons. In contrast, preliminary evidence suggests a much more broadly distributed excitatory input to approximately 70% of tested AP neurons originating from the aortic depressor nerve. These studies provide considerable evidence implicating the AP as a significant neural structure regulating the cardiovascular system.