CENTRAL MECHANISMS OF AREA POSTREMA SYMPATHOINHIBITION

University Of Missouri-Columbia, Columbia MO

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Abstract

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.