CENTRAL MECHANISMS OF AREA POSTREMA SYMPATHOINHIBITION

后脑区产生交感神经抑制反应并增强压力反射介导的交感神经抑制。由于这些作用可能依赖于完整的压力感受器，因此假设静息后区域增强了孤立束核（NITS）的神经传递，孤立束核是压力感受器传入的主要终止部位。谷氨酸被认为是压力感受器传入神经释放的主要神经递质。然而，目前尚不清楚NTS中的谷氨酸神经传递是否需要脑后刺激引起的反应。谷氨酸同时作用于嗜离子性谷氨酸受体（iGluRs）和代谢性谷氨酸受体（mG1uRs），两者都存在于NTS中。虽然iglur对于完整的压力反射是必要的，但mGluR可能调节NTS中的突触谷氨酸传递，正如在其他大脑区域所证明的那样。在NTS中微量注射α 2拮抗剂可消除脑区术后反应。因此，α 2和谷氨酸受体可能在NTS中相互作用，介导区域后期效应。本研究旨在研究谷氨酸（通过iGluRs和mGluRs）和α 2受体在区域后刺激引起的外周和中枢反应中的相互作用。

The area postrema produces sympathoinhibitory responses and enhances baroreflex mediated sympathoinhibition. Since these effects may depend on intact baroreceptors, it has been hypothesized that the area postrema enhances neurotransmission in the nucleus of the solitary tract (NITS), the primary site of baroreceptor afferent termination. Glutamate is thought to be the principal neurotransmitter released by baroreceptor afferents. However, it is unknown if glutamate neurotransmission in the NTS is required for responses elicited by area postrema stimulation. Glutamate acts at both ionotropic glutamate receptors (iGluRs) and metabotropic glutamate receptors (mG1uRs) and both are present in the NTS. While iGluRs are necessary for an intact baroreflex, mGluR may modulate synaptic glutamate transmission in the NTS as has been demonstrated in other brain areas. Microinjections of alpha2 antagonists into the NTS abolish area postrema responses. Thus, alpha2 and glutamate receptors may interact in the NTS to mediate area postrema effects. This proposal is designed to examine interactions of glutamate (through iGluRs and mGluRs) and alpha2 receptors during peripheral and central responses elicited by area postrema stimulation.