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(The FASEB Journal. 2007;21:719.6)
© 2007 FASEB
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719.6

Clonidine-ethanol synergistic behavioral impairment requires activation of central {alpha}2A adrenergic receptors

Tara Summer Bender and Abdel A. Abdel-Rahman

Pharmacology & Toxicology, East Carolina University, 600 Moye Blvd, Greenville, NC, 27834

ABSTRACT

Clonidine-ethanol combination induces synergistic behavioral impairment in rats as measured by rotorod performance and loss of righting reflex (LORR). We tested the hypothesis that the neurochemical effects of ethanol are substantially enhanced by prior activation of central {alpha}2A-adrenergic receptors (AR). Increasing levels of {alpha}2-AR activation (30, 60, and 90 µg/kg clonidine, i.v.) caused proportionate increases in behavioral impairment elicited by ethanol (1 g/kg, i.v.). Possible involvement of the imidazoline (I1) receptor, which is also activated by clonidine, was ruled out by demonstrating the inability of the selective I1 agonist rilmenidine (300 µg/kg, i.v.) to cause behavioral impairment alone or with ethanol. Pharmacological blockade of central {alpha}2A-AR’s (RX821002, 0.3 mg i.c.) abolished the clonidine component of the behavioral response, leaving only the ethanol response, which was similar to ethanol single drug treatment in aCSF controls. By contrast, blockade of central {alpha}2B-AR’s (ARC-239) independently evoked a strong sedative effect. We conclude that activation of central {alpha}2A-AR’s is required to elicit synergistic behavioral impairment by clonidine-ethanol combination. Furthermore, I1 and {alpha}2B-adrenergic receptors, which are also activated by clonidine, do not play a role in this synergistic interaction.

[Supported by NIH grants 5F31AA015472 (TSB) and 2R01AA07839 (ARA)]





This Article
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Right arrow Articles by Bender, T. S.
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Right arrow Articles by Bender, T. S.
Right arrow Articles by Abdel-Rahman, A. A.