.-Autospectral and coherence analyses were used to determine the role of and interactions between paraventricular nucleus (PVN) nitric oxide, ␥-aminobutyric acid (GABA), and the N-methyl-D-aspartic acid (NMDA)-glutamate receptor in regulation of sympathetic nerve discharge (SND) frequency components in anesthetized rats. Four observations were made. First, PVN microinjection of bicuculline (BIC) (GABA A receptor antagonist), but not single PVN injections of NMDA (excitatory amino acid) or N G -monomethyl-L-arginine (L-NMMA; a nitric oxide synthase inhibitor), altered SND frequency components. Second, combined PVN microinjections of L-NMMA and NMDA changed the SND bursting pattern; however, the observed pattern change was different from that produced by PVN BIC and not observed after sinoaortic denervation. Third, PVN microinjection of kynurenic acid prevented and reversed BIC-induced changes in the SND bursting pattern. Finally, vascular resistance (renal and splenic) was significantly increased after PVN BIC microinjection despite the lack of change in the level of renal and splenic SND. These data demonstrate that the PVN contains the neural substrate for altering SND frequency components and suggest complex interactions between specific PVN neurotransmitters and between PVN neurotransmitters and the arterial baroreceptor reflex in SND regulation. coherence function; autospectral analysis; Sprague-Dawley rats; sympathetic nerve discharge THE PARAVENTRICULAR NUCLEUS (PVN) of the hypothalamus is an important central nervous system site for autonomic and neuroendocrine regulation (4,22,32,33). The PVN contains a complex profile of excitatory and inhibitory neurotransmitters and neuromodulators (33). With respect to sympathetic nerve discharge (SND) regulation, PVN glutamate, nitric oxide (NO), and ␥-aminobutyric acid (GABA) have received considerable attention.Ionotropic glutamate receptor subunit mRNAs are expressed in the PVN (10) and glutamate administration into the PVN of conscious rats increases heart rate (HR) (24), arterial pressure (AP) (12, 24), renal SND (12), and plasma norepinephrine concentrations (24).In addition, PVN microinjection of the excitatory amino acid, N-methyl-D-aspartic acid (NMDA), increases renal SND and AP in anesthetized rats (21), suggesting that activation of PVN NMDA receptors is excitatory to SND.The results of several studies (11, 37) suggest that PVN NO is inhibitory to SND. PVN microinjection of nitroprusside, an NO donor, decreases AP (11, 37, 38), HR (37, 38), and renal SND (37, 38), whereas PVN administration of the nitric oxide synthase inhibitor, N G -monomethyl-L-arginine (L-NMMA), increases AP, HR, and renal SND (37). Activation of the NMDA receptor in the PVN releases NO, which inhibits NMDA-mediated increases in SND (21), suggesting interactions between excitatory and inhibitory PVN neurotransmitters in SND regulation.Concerning GABA, several lines of evidence suggest that a PVN GABAergic system tonically inhibits SND (25,26). PVN microinjection of muscimol, a GABA r...
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