The parasubthalamic nucleus (PSTN) projects extensively to the nucleus of the solitary tract (NTS); however, the function of PSTN in cardiovascular regulation is unknown. Experiments were done in
alpha-chloralose anesthetized, paralyzed, and artificially ventilated rats to investigate the effect of
glutamate (10 nl, 0.25 M) activation of PSTN neurons on mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA).
Glutamate stimulation of PSTN elicited depressor (-20.4 +/- 0.7 mmHg) and
bradycardia (-26.0 +/- 1.0 beats/min) responses and decreases in RSNA (67 +/- 17%).
Administration (intravenous) of
atropine methyl bromide attenuated the
bradycardia response (46%), but had no effect on the MAP response. Subsequent
intravenous administration of
hexamethonium bromide blocked both the remaining
bradycardia and depressor responses. Bilateral microinjection of the synaptic blocker
CoCl(2) into the caudal NTS region attenuated the PSTN depressor and
bradycardia responses by 92% and 94%, respectively. Additionally, prior
glutamate activation of neurons in the ipsilateral NTS did not alter the magnitude of the MAP response to stimulation of PSTN, but potentiated HR response by 35%. Finally, PSTN stimulation increased the magnitude of the reflex
bradycardia to activation of arterial baroreceptors. These data indicate that activation of neurons in the PSTN elicits a decrease in MAP due to sympathoinhibition and a cardiac slowing that involves both vagal excitation and sympathoinhibition. In addition, these data suggest that the PSTN depressor effects on circulation are mediated in part through activation of NTS neurons involved in baroreflex function.