Clonidine inhibits electrodermal responses by an action on the spinal cord

European Journal of Pharmacology
M C Koss, J A Hey

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 micrograms 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 micrograms i.a.). Intravenous clonidine (1-30 micrograms) 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 alpha 2-adrenoceptors in the spinal cord and to a limited extent by direct action at the neuroeffector junction. Although a possible DMPP-clonidine intera...Continue Reading

References

Jul 15, 1977·European Journal of Pharmacology·T Baum, A T Shropshire
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Nov 10, 1976·Psychopharmacology·M C KossP J Bernthal
Nov 1, 1976·Naunyn-Schmiedeberg's Archives of Pharmacology·M C Koss, M A Davison
May 1, 1976·European Journal of Pharmacology·M C Koss, M A Davison
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Citations

Jul 3, 1990·European Journal of Pharmacology·M C KossT Ito
Jun 3, 2015·European Journal of Pain : EJP·L Vo, P D Drummond

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