Involvement of central amygdala NMDA receptor mechanism in morphine state-dependent memory retrieval.

In the current study, the effects of intra-central amygdala (CeA) administration of N-methyl-D-aspartate (NMDA) and its competitive antagonist, D-2-amino-5-phosphonopentanoic acid (D-AP5), on morphine state-dependent memory retrieval were investigated. Post-training subcutaneous (s.c.) administration of different doses of morphine (0.5, 2.5, 5 and 7.5 mg/kg) dose-dependently impaired memory. The response induced by post-training morphine (7.5 mg/kg) was reversed by pre-test administration of this drug (5 and 7.5 mg/kg), indicating morphine state-dependent memory retrieval. Pre-test intra-CeA administration of NMDA (0.01 and 0.05 μg/rat) plus an ineffective dose of morphine (0.5 mg/kg, s.c.) restored memory impairment caused by post-training morphine (7.5 mg/kg). However, pre-test intra-CeA administration of NMDA (0.005-0.05 μg/rat), alone, was ineffective on post-training morphine-induced amnesia. Furthermore, pre-test intra-CeA administration of the same doses of NMDA had no effect on memory retrieval. Pre-test intra-CeA administration of D-AP5 (0.1-1.0 μg/rat) decreased morphine state-dependent memory retrieval. However, pre-test administration of D-AP5 (0.1-1 μg/rat) alone decreased memory retrieval, but restored post-training morphine-induced amnesia. In conclusion, our results suggest which CeA may be potentially critical for morphine state-dependent memory retrieval and that CeA NMDA receptor mechanism(s) interact with the opiodergic system in the modulation of morphine state-dependent memory retrieval.