Noradrenergic neurotransmission at PVN in locus ceruleus-induced baroreflex suppression in rats.

We investigated the role of ascending noradrenergic projections from the locus ceruleus (LC) to the paraventricular nucleus (PVN) of the hypothalamus in LC-induced suppression of the baroreceptor reflex (BRR) response in adult Sprague-Dawley rats maintained under pentobarbital anesthesia. On the basis of in vivo microdialysis and high-performance liquid chromatography-electrochemical detection, microinjection of L-glutamate (5 nmol) into the LC resulted in a site-specific increase in norepinephrine (NE) concentration in the dialysate collected from the parvocellular subnucleus of the PVN. The temporal course of this increase in extracellular NE concentration in the PVN coincided with the time course of inhibition elicited by the LC on the BRR response. Microinfusion of NE (10, 50, or 100 nM) into the parvocellular subnucleus of the PVN by reverse microdialysis also promoted a parallel increase in NE at the PVN and a reduction in the BRR response. Inhibition of the BRR response induced by microinjection into the PVN of the alpha 1-adrenoceptor agonist phenylephrine (10 nmol) or chemical activation of the LC was reversed by bilateral PVN microinjection of prazosin (100 pmol). However, local application to the PVN of the alpha 2- or beta-adrenoceptor agonist guanabenz (10 nmol) or isoproterenol (10 nmol) was ineffective. Our results suggest that NE released from the LC-PVN noradrenergic projection may participate in LC-induced suppression of the BRR response by activating the alpha 1-adrenoceptors at the parvocellular subnucleus of the PVN.