Clonidine inhibits electrodermal responses by an action on the spinal cord

Abstract

Experiments were designed to determine the neural site of action for clonidine inhibition of sympathetic-cholinergic electrodermal responses (EDR) in anesthetized cats. Administration of clonidine (0.3–3.0 μg i.a.) directly to the stellate ganglion did not significantly decrease the amplitude of responses evoked by submaximal hypothalamic stimulation but did inhibit hypothalamic-evoked EDR when administered intrathecally at the C6 to T2 spinal levels. Administration of clonidine to the ganglion, however, did depress EDR evoked by the ganglionic stimulant, 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP, 10 μg i.a.). Intravenous clonidine (1–30 μg) also reduced EDR amplitude evoked by single pulse stimulation of both the pre- and postganglionic sympathetic nerves with responses elicited from both sites depressed to an equal extent. Yohimbine (0.5 mg/kg i.v.) uniformly antagonized clonidine's depression of EDR regardless of the site or mode of activation. These results indicate that clonidine depresses centrally evoked sudomotor responses by activation of α 2-adrenoceptors in the spinal cord and to a limited extent by direct action at the neuroeffector junction. Although a possible DMPP-clonidine interaction appears to take place at the level of the sympathetic ganglion, it is unlikely that ganglionic blockade contributes significantly to clonidine inhibition of EDR evoked by electrical activation of the nervous system.