Stimulation of alpha(1)-adrenoceptors inhibits memory consolidation in thechick

Investigation of the effects of the different adrenoceptor (AR) subtypes in memory formation may reveal discrete actions of noradrenaline in memory mo dulation and storage mediated through particular AR subtypes. Noradrenaline injected intracerebrally in the chick produced biphasic effects on memory consolidation with enhancement at low doses and inhibition at high doses. W e have previously shown that the enhancement by the lower doses of noradren aline is attributable to actions at beta (2)- and beta (3)-adrenoceptors, w hereas the inhibitory effect of higher doses is attributable to alpha (1)-a drenoceptors. The present studies show that the inhibition of memory by hig h doses of noradrenaline is mimicked by the alpha (1)-AR agonist methoxamin e, and the dose-response curve is shifted to the right by pretreatment with the alpha (1)-AR antagonist prazosin. alpha (1)-ARs may play a critical ro le in memory formation in highly stressful situations, when noradrenaline l evels are high in particular brain regions. It is not known where the alpha (1)-ARs responsible for the effect on memory are localized. alpha (1)-ARs are found on neurons and astrocytes and in the cerebral vasculature and the refore the action of high doses of noradrenaline via alpha (1)-AR agonists could be via an action at any of these sites. Activation of alpha (1)-adren oceptors in the intermediate hyperstriatum ventrale in the chick forebrain by the alpha (1) adrenoceptor agonist methoxamine inhibits the consolidatio n of memory. Because the same effect is produced by high levels of noradren aline, it is likely that stimulation of alpha (1)-ARs is the mechanism unde rlying this effect.