Investigation of the effects of the different adrenoceptor (AR) subtypes in memory formation may reveal discrete actions of noradrenaline in memory modulation 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. We have previously shown that the enhancement by the lower doses of noradrenaline is attributable to actions at β2- and β3-adrenoceptors, whereas the inhibitory effect of higher doses is attributable to α1-adrenoceptors. The present studies show that the inhibition of memory by high doses of noradrenaline is mimicked by the α1-AR agonist methoxamine, and the dose-response curve is shifted to the right by pretreatment with the α1-AR antagonist prazosin. α1-ARs may play a critical role in memory formation in highly stressful situations, when noradrenaline levels are high in particular brain regions. It is not known where the α1-ARs responsible for the effect on memory are localized. α1-ARs are found on neurons and astrocytes and in the cerebral vasculature and therefore the action of high doses of noradrenaline via α1-AR agonists could be via an action at any of these sites. Activation of α1-adrenoceptors in the intermediate hyperstriatum ventrale in the chick forebrain by the α1 adrenoceptor agonist methoxamine inhibits the consolidation of memory. Because the same effect is produced by high levels of noradrenaline, it is likely that stimulation of α1-ARs is the mechanism underlying this effect.
- Discriminated avoidance learning
- Memory inhibition