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首页> 外文期刊>American Journal of Physiology >Viscerosensory input drives angiotensin II type 1A receptor-expressing neurons in the solitary tract nucleus
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Viscerosensory input drives angiotensin II type 1A receptor-expressing neurons in the solitary tract nucleus

机译：粘滞输入驱动血管紧张素II型1A型孤独核中的表达的神经元

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摘要

Homeostatic regulation of visceral organ function requires integrated processing of neural and neurohormonal sensory signals. The nucleus of the solitary tract (NTS) is the primary sensory nucleus for cranial visceral sensory afferents. Angiotensin II (ANG II) is known to modulate peripheral visceral reflexes, in part, by activating ANG II type 1A receptors (AT_(1A)R) in the NTS. AT_(1A)R-expressing NTS neurons occur throughout the NTS with a defined subnuclear distribution, and most of these neurons are depolarized by ANG II. In this study we determined whether AT_(1A)R-expressing NTS neurons receive direct visceral sensory input, and whether this input is modulated by ANG II. Using AT_(1A)R-GFP mice to make targeted whole cell recordings from AT_(1A)R-expressing NTS neurons, we demonstrate that two-thirds (37 of 56) of ATiAR-expressing neurons receive direct excitatory, visceral sensory input. In half of the neurons tested (4 of 8) the excitatory visceral sensory input was significantly reduced by application of the transient receptor potential vallinoid type 1 receptor agonist, capsaicin, indicating AT_(1A)R-expressing neurons can receive either C- or A-fiber-mediated input. Application of ANG II to a subset of second-order AT_(1A)R-expressing neurons did not affect spontaneous, evoked, or asynchronous glutamate release from visceral sensory afferents. Thus it is unlikely that AT_(1A)R-expressing viscerosensory neurons terminate on AT_(1A)R-expressing NTS neurons. Our data suggest that ANG II is likely to modulate multiple visceral sensory modalities by altering the excitability of second-order AT_(1A)R-ex-pressing NTS neurons.
机译：内脏器官功能的稳态调节需要综合处理神经和神经异常感觉信号。孤子道（NTS）的核是颅骨内脏感觉传入的主要感觉核。已知血管紧张素II（Ang II）通过在NTS中激活Ang II型1A受体（AT_（1A）R）来调节外周内脏反射。 AT_（1A）在具有定义的亚核分布的NTS中，在整个NT中发生r-EXT表达NTS神经元，并且大多数这些神经元通过ANG II去极化。在该研究中，我们确定了AT_（1A）是否表达NTS神经元接收直接内脏感觉输入，以及该输入是否通过ANG II调制。使用AT_（1A）R-GFP小鼠从AT_（1A）表达的NTS神经元进行靶向整个细胞录制，我们证明了三分之二（37个中的37个中的37％）的目的地神经元接受直接兴奋性的内脏感官输入。在测试的一半神经元（8个中的）（4个中的4个）通过施加瞬态受体潜在的vallinoid型1受体激动剂辣椒素显着降低了兴奋性内脏感觉输入，表明AT_（1A）表达的神经元可以接受C-或A. - 介导的输入。 Ang II在二阶AT_（1A）r-表达神经元的施加不影响来自内脏感官传入的自发性，诱发或异步谷氨酸释放。因此，AT_（1A）r-表达的岩浆病神经元不太可能终止于AT_（1A）r-表达NTS神经元。我们的数据表明，Ang II可能通过改变二阶AT_（1A）R-EXCHED NTS神经元的兴奋性来调节多个内脏感官模态。

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