CENTRAL MECHANISMS OF AREA POSTREMA SYMPATHOINHIBITION

最后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，因此有人假设最后区增强了孤束核（NITS）中的神经传递，NITS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神经释放的主要神经递质。 然而，它是未知的，如果谷氨酸在NTS的神经传递所需的最后区刺激引起的反应。 谷氨酸作用于离子型谷氨酸受体（iGluRs）和代谢型谷氨酸受体（mGluRs），两者都存在于NTS中。 虽然iGluR对于完整的压力感受器反射是必需的，但是mGluR可以调节NTS中的突触谷氨酸传递，如已经在其他脑区域中证明的。将α 2拮抗剂微量注射到NTS中可消除最后区反应。 因此，α 2和谷氨酸受体可能在NTS中相互作用以介导最后区效应。 该提议旨在研究谷氨酸（通过iGluRs和mGluRs）和α 2受体在最后区刺激引起的外周和中枢反应期间的相互作用。

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.