Consolidation of a weakly reinforced memory that would otherwise fade after 30 min can be achieved by central or peripheral injection of the selective beta(3)-adrenoceptor agonist CL316243 as well as the beta(2)-adrenoceptor agonist zinterol and the alpha(1)-adrenoceptor antagonist prazosin in the day-old chick. The effect of the beta(3)-adrenoceptor agonist is mimicked by peripheral or central injection of glucose that is effective in enhancing memory from 25 min before to 25 min after training. Glucose uptake into various cell types has been described following activation of beta(3)-adrenoceptors and in this paper we demonstrate that activation of beta(3)-adrenoceptors by CL316243 facilitates the effect of a dose of glucose that does not normally enhance memory, whereas a beta(2)-adrenoceptor agonist and an alpha(1)-adrenoceptor antagonist have no effect. Administration of the glucose uptake inhibitor 2-deoxyglucose prevented the consolidation of strongly reinforced training. The beta(3)-adrenoceptor agonist facilitated the effect of a non-amnestic dose of 2-deoxyglucose to inhibit memory. There are two time periods relative to the learning trial where memory is vulnerable to interference by centrally administered 2-deoxyglucose: one related to short-term memory and one at the time of consolidation into long-term memory. Peripheral injection of 2-deoxyglucose is only effective at the time of consolidation. The action of the beta(3)-adrenoceptor agonist to facilitate the action of 2-deoxyglucose only occurs at the time of consolidation. We suggest that a noradrenergic agonist acting at beta(3)-adrenoceptors enhances memory formation by facilitation of glucose uptake at the time of memory consolidation. This may represent a novel mechanism that would be beneficial for developing compounds for the facilitation of memory in diseases with cognitive deficits.