Effect of clonidine and gamma-aminobutyric acid on the discharges of medullo-spinal sympathoexcitatory neurons in the rat.

Single-unit recordings of 50 pressure-sensitive neurons with axonal projections to the thoracic spinal cord were obtained in the retrofacial portion of nucleus paragigantocellularis lateralis of halothane-anesthetized rats. Two types of cells were distinguished on the basis of their axonal conduction velocities: a slow-conducting (mean 0.6 m/s, group I) and a fast-conducting one (group II, mean 3.3 m/s). Both cell types were completely silenced by elevating mean arterial pressure above 160 mm Hg by means of aortic constriction and exhibited a plateau of high spontaneous activity below 70 mm Hg. Only group I neurons were significantly inhibited by the administration of clonidine in a dose producing 90% of its maximum hypotensive effect (11.5 micrograms/kg, i.v.). Hypotensive doses of clonidine administered into the fourth ventricle also produced a selective inhibition of group I neurons, while the others were unaffected. Iontophoretic applications of clonidine and norepinephrine produced an inhibition of the discharges of group I neurons qualitatively and quantitatively identical to that observed following administration of clonidine by the i.v. or i.c.v. route. Once more, group II cells were unaffected. In contrast, iontophoretically applied gamma-aminobutyric acid exerted a powerful inhibition of both cell types, an effect which was totally prevented or reversed by the gamma-aminobutyric acid antagonist bicuculline. Anatomical experiments were performed to uncover the potential source of catecholaminergic innervation of the area in which recordings were obtained. This area contains a large number of adrenaline-synthesizing neurons and receives a selective noradrenergic input from the A5 pontine group with no contribution from the A1, A2, A6 and A7 brainstem clusters of noradrenergic cells.