is likely that acute hypotensive/sedating effects, which are known to be associated with high doses of clonidine, contributed to the profound clonidine-induced suppression of alcohol consumption. It has been reported that when a bolus intravenous (IV) injection of clonidine was followed immediately (within 10 min) by an IV injection of 1 g alcohol/kg BW, clonidine acutely increased alcohol-induced sedation by an α2A-adrenergic receptor-mediated mechanism (Bender & Abdel-Rahman, 2009). Hence, it also is possible that the high (80 µg/kg) dose of clonidine enhanced the acute sedating effects of alcohol, thus leading to a cessation of alcohol drinking early in the 2-h alcohol-access period. Recent evidence suggests that some α2-agonist effects, including sedation, can be mediated by α2-adrenoceptor receptors located on non-adrenergic cells rather than by autoreceptor-mediated inhibition of norepinephrine release (Gilsbach et al., 2009).
