CENTRAL MECHANISMS OF AREA POSTREMA SYMPATHOINHIBITION

最后区产生交感抑制反应，并增强压力感受性反射介导的交感抑制。由于这些效应可能依赖于完整的压力感受器，因此假设最后区增强了孤束核(NITS)的神经传递，孤束核是压力感受器传入终止的主要部位。谷氨酸被认为是压力感受器传入释放的主要神经递质。然而，刺激后脑区的反应是否需要NTS中的谷氨酸神经传递尚不清楚。谷氨酸既作用于离子型谷氨酸受体(IGluRs)，也作用于代谢型谷氨酸受体(MG1uRs)，两者均存在于NTS。虽然iGluR是一个完整的压力感受器反射所必需的，但mGluR可能会调节NTS中突触的谷氨酸传递，正如在其他大脑区域所证明的那样。NTS区微量注射α2拮抗剂可消除最后区反应。因此，α2和谷氨酸受体可能在孤束核内相互作用，以调节区域的后遗症效应。这项建议旨在研究谷氨酸(通过iGluRs和mGluRs)和Alpha2受体在刺激后脑区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.