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Modulation of ethanol state-dependent learning by dorsal hippocampal NMDA receptors in mice.
Alcohol. 2008 Dec; 42(8):667-74.A

Abstract

The possible role of N-methyl-D-aspartate (NMDA) receptors of dorsal hippocampus on ethanol state-dependent learning was studied in adult male mice (Pasteur Institute, Iran). As a model of memory, a single-trial step-down passive avoidance task was used. All animals were bilaterally implanted with cannulae into the CA1 regions of dorsal hippocampi. Results show that intraperitoneal (i.p.) administration of ethanol (0.5 and 1 g/kg) 30 min before training impaired memory performance in animals when tested 24h later. Pretest administration of the same doses of ethanol-induced state-dependent retrieval of the memory acquired under pretraining ethanol (1 g/kg, i.p.) influence. Pretest intra-CA1 microinjection of NMDA (0.001, 0.01, and 0.1 microg/mouse) by itself had no effect on memory retrieval and ethanol-induced amnesia. However, pretest intra-CA1 administration of the same doses of NMDA with an ineffective dose of ethanol (0.25 g/kg, i.p.) significantly restored the retrieval and potentiated ethanol state-dependent learning. On the other hand, pretest administration of a competitive NMDA receptor antagonist D-AP5 (D-(-)-2-Amino-5-phosphonopentanoic acid) (0.01, 0.1, and 1 microg/mouse, intra-CA1) or a noncompetitive NMDA receptor antagonist MK-801 maleate [(5S, 10R)-(+)-5-Methyl-10, 11-dihydro-5H-dibenzo [a, d] cyclohepten-5, 10-imine maleate] (0.25, 0.5, and 1 g/mouse, intra-CA1) 5 min before the administration of ethanol (1 g/kg, i.p.) significantly inhibited ethanol state-dependent learning. Intra-CA1 pretest administration of D-AP5 (0.01, 0.1, and 1 microg/mouse) or MK-801 maleate [5S, 10R)-(+)-5-Methyl-10, 11-dihydro-5H-dibenzo [a, d] cyclohepten-5, 10-imine maleate] (0.25, 0.5, and 1 microg/mouse) alone did not affect memory retention. It may be concluded that dorsal hippocampal NMDA receptors are involved in mediating ethanol state-dependent learning.

Authors+Show Affiliations

Department of Animal Biology, School of Biology, College of Science, University of Tehran, P. O. Box 4155-6455, Tehran, Iran. rezayof@khayam.ut.ac.irNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18774674

Citation

Rezayof, Ameneh, et al. "Modulation of Ethanol State-dependent Learning By Dorsal Hippocampal NMDA Receptors in Mice." Alcohol (Fayetteville, N.Y.), vol. 42, no. 8, 2008, pp. 667-74.
Rezayof A, Sharifi K, Zarrindast MR, et al. Modulation of ethanol state-dependent learning by dorsal hippocampal NMDA receptors in mice. Alcohol. 2008;42(8):667-74.
Rezayof, A., Sharifi, K., Zarrindast, M. R., & Rassouli, Y. (2008). Modulation of ethanol state-dependent learning by dorsal hippocampal NMDA receptors in mice. Alcohol (Fayetteville, N.Y.), 42(8), 667-74. https://doi.org/10.1016/j.alcohol.2008.05.005
Rezayof A, et al. Modulation of Ethanol State-dependent Learning By Dorsal Hippocampal NMDA Receptors in Mice. Alcohol. 2008;42(8):667-74. PubMed PMID: 18774674.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Modulation of ethanol state-dependent learning by dorsal hippocampal NMDA receptors in mice. AU - Rezayof,Ameneh, AU - Sharifi,Khadijeh, AU - Zarrindast,Mohammad-Reza, AU - Rassouli,Yassaman, Y1 - 2008/09/06/ PY - 2007/11/09/received PY - 2008/05/09/revised PY - 2008/05/23/accepted PY - 2008/9/9/pubmed PY - 2009/2/6/medline PY - 2008/9/9/entrez SP - 667 EP - 74 JF - Alcohol (Fayetteville, N.Y.) JO - Alcohol VL - 42 IS - 8 N2 - The possible role of N-methyl-D-aspartate (NMDA) receptors of dorsal hippocampus on ethanol state-dependent learning was studied in adult male mice (Pasteur Institute, Iran). As a model of memory, a single-trial step-down passive avoidance task was used. All animals were bilaterally implanted with cannulae into the CA1 regions of dorsal hippocampi. Results show that intraperitoneal (i.p.) administration of ethanol (0.5 and 1 g/kg) 30 min before training impaired memory performance in animals when tested 24h later. Pretest administration of the same doses of ethanol-induced state-dependent retrieval of the memory acquired under pretraining ethanol (1 g/kg, i.p.) influence. Pretest intra-CA1 microinjection of NMDA (0.001, 0.01, and 0.1 microg/mouse) by itself had no effect on memory retrieval and ethanol-induced amnesia. However, pretest intra-CA1 administration of the same doses of NMDA with an ineffective dose of ethanol (0.25 g/kg, i.p.) significantly restored the retrieval and potentiated ethanol state-dependent learning. On the other hand, pretest administration of a competitive NMDA receptor antagonist D-AP5 (D-(-)-2-Amino-5-phosphonopentanoic acid) (0.01, 0.1, and 1 microg/mouse, intra-CA1) or a noncompetitive NMDA receptor antagonist MK-801 maleate [(5S, 10R)-(+)-5-Methyl-10, 11-dihydro-5H-dibenzo [a, d] cyclohepten-5, 10-imine maleate] (0.25, 0.5, and 1 g/mouse, intra-CA1) 5 min before the administration of ethanol (1 g/kg, i.p.) significantly inhibited ethanol state-dependent learning. Intra-CA1 pretest administration of D-AP5 (0.01, 0.1, and 1 microg/mouse) or MK-801 maleate [5S, 10R)-(+)-5-Methyl-10, 11-dihydro-5H-dibenzo [a, d] cyclohepten-5, 10-imine maleate] (0.25, 0.5, and 1 microg/mouse) alone did not affect memory retention. It may be concluded that dorsal hippocampal NMDA receptors are involved in mediating ethanol state-dependent learning. SN - 1873-6823 UR - https://www.unboundmedicine.com/medline/citation/18774674/Modulation_of_ethanol_state_dependent_learning_by_dorsal_hippocampal_NMDA_receptors_in_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0741-8329(08)00263-2 DB - PRIME DP - Unbound Medicine ER -