Sun M K, Reis D J
Department of Neurology and Neuroscience, Cornell University Medical College, New York, NY 10021, USA.
Eur J Pharmacol. 1995 Apr 4;276(3):291-6. doi: 10.1016/0014-2999(95)00095-3.
In vitro, clonidine (1, 10, or 30 microM) dose-dependently and reversibly inhibited tonically active pacemaker neurons that correspond to the relatively fast-conducting reticulospinal vasomotor neurons of the rostral ventrolateral reticular nucleus of the medulla oblongata in rats. The clonidine-induced membrane-hyperpolarizing response of these neurons was abolished by either tetrodotoxin, bicuculline, a GABAA receptor antagonist, or 4,4'-diisothiocyano-1,2'-disulphonic stilbene acid, a Cl- channel blocker. We conclude that the clonidine-induced inhibition of the pacemaker neurons of the rostral ventrolateral reticular nucleus is indirect, mediated by synaptic release of gamma-aminobutyric acid (GABA) or GABA-like substances, which activate Cl- channels of the pacemaker neurons of the rostral ventrolateral reticular nucleus.