Abstract
Interactions between cannabinoid and glutamate systems have been demonstrated in some brain areas associated with mnemonic functions. This study investigates the effects of bilateral post-training intra-nucleus accumbens (NAc) shell administrations of glutamate NMDA receptor agents on memory impairment induced by cannabinoid CB1 receptor activation during a step-through inhibitory avoidance (IA) task. Our results showed post-training administration of ACPA (CB1 receptor agonist; 3ng/side) impairs IA memory consolidation, whereas AM251 (CB1 receptor antagonist; 0.3, 3 and 30ng/side), NMDA (0.3, 3 and 30ng/side), and d-AP7 (NMDA receptor antagonist; 3, 30 and 300ng/side) were ineffective. However, co-administration of AM251 (30ng/side) or NMDA (30ng/side) with ACPA (3ng/side) prevented the memory-impairing effect of ACPA. Meanwhile, co-administration of NMDA (30ng/side) and a subthreshold dose of ACPA (0.15ng/side) decreased memory consolidation. Moreover, post-training microinjection of AM251 (30ng/side) or d-AP7 (300ng/side) prevented memory impairment induced by co-administration of subthreshold doses of NMDA and ACPA. The data indicated that NMDA receptor mechanism(s), at least partly, play(s) a role in modulating the effect of ACPA on memory consolidation in the NAc shell.
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