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1 Division of Basic Biomedical Science, Univerisity of South Dakota, Vermillion, United States
2 Department of Psychiatry, University of Cincinnati, Cincinnati, Ohio, United States
3 Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska, United States
* To whom correspondence should be addressed. E-mail: kpatel{at}unmc.edu.
Paraventricular nucleus of hypothalamus (the PVN) is a central site known to modulate sympathetic outflow. Both excitatory and inhibitory neurotransmitters within the PVN dictate final outflow. The goal of the present study was to examine the role of the interaction of excitatory neurotransmitter, glutamate and inhibitory neurotransmitter, GABA in regulating sympathetic activity. In 
-chloralose and urethane anesthetized rats, microinjection of glutamate and NMDA into the PVN (50, 100 and 200 pmol) produced dose-dependent increases in RSNA, BP and HR. These responses were blocked by the NMDA receptor antagonist AP-5. Additionally, microinjection of bicuculline, a GABAA receptor antagonist, into the PVN (50, 100 and 200 pmol) also produced significant, dose-dependent increases in RSNA, BP and HR. The NMDA receptor antagonist AP-5 also blocked these responses. Furthermore, using microdialysis and HPLC/EC techniques, it was observed that infusing bicuculline into the PVN caused an increase in glutamate release. Finally, using an in vitro hypothalamic slice preparation, we found that bicuculline increased the frequency of glutamate-mediated EPSCs in PVN-RVLM projecting neurons, supporting a GABAA-mediated tonic inhibition of this excitatory input into these neurons. Altogether, these data indicate that 1) glutamate, via NMDA receptors, excites the pre-sympathetic neurons within the PVN and increase sympathetic outflow and 2) this glutamate excitatory input is tonically inhibited by a GABAA-mediated mechanism.
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