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Involvement of central amygdala NMDA receptor mechanism in morphine state-dependent memory retrieval.
Neurosci Res. 2011 Jan; 69(1):25-31.NR

Abstract

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.

Authors+Show Affiliations

Institute for Cognitive Science Studies, Tehran, Iran.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

20875463

Citation

Ardjmand, Abolfazl, et al. "Involvement of Central Amygdala NMDA Receptor Mechanism in Morphine State-dependent Memory Retrieval." Neuroscience Research, vol. 69, no. 1, 2011, pp. 25-31.
Ardjmand A, Rezayof A, Zarrindast MR. Involvement of central amygdala NMDA receptor mechanism in morphine state-dependent memory retrieval. Neurosci Res. 2011;69(1):25-31.
Ardjmand, A., Rezayof, A., & Zarrindast, M. R. (2011). Involvement of central amygdala NMDA receptor mechanism in morphine state-dependent memory retrieval. Neuroscience Research, 69(1), 25-31. https://doi.org/10.1016/j.neures.2010.09.005
Ardjmand A, Rezayof A, Zarrindast MR. Involvement of Central Amygdala NMDA Receptor Mechanism in Morphine State-dependent Memory Retrieval. Neurosci Res. 2011;69(1):25-31. PubMed PMID: 20875463.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Involvement of central amygdala NMDA receptor mechanism in morphine state-dependent memory retrieval. AU - Ardjmand,Abolfazl, AU - Rezayof,Ameneh, AU - Zarrindast,Mohammad-Reza, Y1 - 2010/09/25/ PY - 2010/05/20/received PY - 2010/08/25/revised PY - 2010/09/14/accepted PY - 2010/9/30/entrez PY - 2010/9/30/pubmed PY - 2011/6/22/medline SP - 25 EP - 31 JF - Neuroscience research JO - Neurosci Res VL - 69 IS - 1 N2 - 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. SN - 1872-8111 UR - https://www.unboundmedicine.com/medline/citation/20875463/Involvement_of_central_amygdala_NMDA_receptor_mechanism_in_morphine_state_dependent_memory_retrieval_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0168-0102(10)02804-X DB - PRIME DP - Unbound Medicine ER -