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大鼠孤束核中NK1受体的消融会阻断压力反射。

Ablation of NK1 receptors in rat nucleus tractus solitarii blocks baroreflexes.

作者信息

Riley Jeffrey, Lin Li-Hsien, Chianca Deoclecio A, Talman William T

机构信息

Laboratory of Neurobiology, Department of Neurology, University of Iowa and Veterans Affairs Medical Center, Iowa City 52242, USA.

出版信息

Hypertension. 2002 Dec;40(6):823-6. doi: 10.1161/01.hyp.0000042089.34004.cf.

Abstract

The neuropeptide substance P (SP) is found in vagal afferent nerves within the nucleus tractus solitarii, where it is released on stimulation of arterial baroreflexes. The neurokinin-1 receptors at which SP may act have been identified in the nucleus tractus solitarii, but there remains uncertainty if the neurons at which SP acts are critical to baroreflex transmission. By using SP conjugated with the toxin saporin, which kills the neurons at which SP may act, we sought to test the hypothesis that neurons expressing the neurokinin-1 receptor are critical to baroreflex transmission in the nucleus tractus solitarii. One and 2 weeks after injection of the toxin into the rat nucleus tractus solitarii, immunoreactivity for the neurokinin-1 receptor was lost. When the toxin had been injected bilaterally, the baroreflex gain was significantly reduced. Therefore, neurons that express SP receptors play a critical role in mediating baroreflexes through the nucleus tractus solitarii of rat.

摘要

神经肽P物质(SP)存在于孤束核内的迷走传入神经中,在动脉压力反射受到刺激时会在此处释放。孤束核中已鉴定出SP可能作用的神经激肽-1受体,但SP作用的神经元对压力反射传递是否至关重要仍不确定。通过使用与毒素皂草素结合的SP,该毒素可杀死SP可能作用的神经元,我们试图验证表达神经激肽-1受体的神经元对孤束核压力反射传递至关重要这一假设。将毒素注射到大鼠孤束核1周和2周后,神经激肽-1受体的免疫反应性消失。当双侧注射毒素时,压力反射增益显著降低。因此,表达SP受体的神经元在通过大鼠孤束核介导压力反射中起关键作用。

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