Abstract
This study demonstrates a role for α2-adrenoceptors in the basal ganglia in the consolidation of memory using weakly and strongly reinforced models of discriminated avoidance learning in the chick. The memory enhancing action of noradrenaline injected into the basal ganglia (lobus parolfactorius—LPO) was reduced in the presence of the α2-adrenoceptor antagonist yohimbine, but when noradrenaline was injected into the multi-modal association area (intermediate medial hyperstriatum ventrale—IMHV), yohimbine failed to prevent memory enhancement.Yohimbine injected into the LPO prevented, whereas the α2-adrenoceptor agonists oxymetazoline and clonidine enhanced, consolidation of memory. The timing of the inhibitory effect of yohimbine in the LPO suggested that α2-adrenoceptor involvement occurs 10–15 min after training, and that stimulation of α2-ARs in LPO is necessary for subsequent consolidation of memory. Oxymetazoline, being hydrophilic, was ineffective injected into IMHV, whereas the action of the lipophilic α2-adrenoceptor agonist clonidine in the IMHV was interpreted as an action at a site more distal in the brain, probably the LPO.The results suggest that noradrenaline release in the basal ganglia in the chick stimulates α2-adrenoceptors, which modulate and consolidate memory formation mediated by β2- or β3-ARs in the association area. The LPO may be responsible for the reinforcement of memory in the IMHV.
Published Version
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