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| Paper IPM / Cognitive / 12165 |
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| Abstract: | |||||||
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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 0.05g/rat) plus an ineffective dose of morphine (0.5 mg/kg, s.c.)
restoredmemoryimpairment caused by post-training morphine (7.5 mg/kg). However, pre-test intra-CeA
administration of NMDA (0.005?0.05g/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?1.0g/rat) decreased morphine statedependent
memory retrieval. However, pre-test administration of D-AP5 (0.1?1g/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.
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