The electrodermal response as a model for central sympathetic reactivity: The action of clonidine

Abstract

Electrodermal responses (EDR) were evoked centrally by stimulation of reactive loci in the posterior hypothalamus and peripherally by stimulation of the distal portion of the sectioned median or ulnar nerve. Moderate doses of clonidine (3–30 μg/kg, i.v.) reduced the amplitude of the centrally evoked EDR while having no effect on the peripherally evoked responses. This central action of clonidine occured concomitantly with the clonidine-induced bradycardia and hypotension. Administration of clonidine shifted the centrally evoked EDR frequency-response to the right in a dose related manner at 3, 10 and 30 μg/kg, i.v. 1 μg/kg was without effect on these responses. This central depressant action of clonidine was partially reversed following administration of yohimbine (0.5–1.0 μg/kg, i.v.). These results suggest that clonidine inhibits central reactivity in this sympathetic-cholinergic system in a manner analogous to its action on other sympathetic systems, and that a central adrenergic inhibitory mechanism may be involved.