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Nicotine improves ethanol-induced memory impairment: the role of dorsal hippocampal NMDA receptors.
Life Sci. 2010 Feb 13; 86(7-8):260-6.LS

Abstract

AIMS

The current study was undertaken to determine the role of dorsal hippocampal N-methyl-d-aspartate (NMDA) receptors in nicotine's effect on impairment of memory by ethanol.

MAIN METHODS

Adult male mice were cannulated in the CA1 regions of dorsal hippocampi and trained on a passive avoidance learning task for memory assessment.

KEY FINDINGS

We found that pre-training intraperitoneal (i.p.) administration of ethanol (0.5 and 1g/kg) decreased memory retrieval when tested 24h later. Pre-test administration of ethanol reversed the decrease in inhibitory avoidance response induced by pre-training ethanol. Similar to ethanol, pre-test administration of nicotine (0.125-0.75 mg/kg, s.c.) prevented impairment of memory by pre-training ethanol. In the animals that received ethanol (1g/kg, i.p) before training and tested following intra-CA1 administration of different doses of NMDA (0.0005-0.005 microg/mouse), no significant change was observed in the retrieval latencies. Co-administration of the same doses of NMDA with an ineffective dose of nicotine (0.125 mg/kg, s.c.) significantly improved the memory retrieval and mimicked the effects of pre-test administration of a higher dose of nicotine. Pre-test intra-CA1 microinjection of MK-801 (0.25-1 microg/mouse), which had no effect alone, in combination with an effective dose of nicotine (0.75 mg/kg, s.c.) prevented the improving effect of nicotine on memory impaired by pre-training ethanol. Moreover, intra-CA1 microinjection of MK-801 reversed the NMDA-induced potentiation of the nicotine response.

SIGNIFICANCE

The results suggest the importance of NMDA glutamate system(s) in the CA1 regions of dorsal hippocampus for improving the effect of nicotine on the ethanol-induced amnesia.

Authors+Show Affiliations

Department of Animal Biology, School of Biology, College of Science, University of Tehran, 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

20035769

Citation

Rezayof, Ameneh, et al. "Nicotine Improves Ethanol-induced Memory Impairment: the Role of Dorsal Hippocampal NMDA Receptors." Life Sciences, vol. 86, no. 7-8, 2010, pp. 260-6.
Rezayof A, Shirazi-Zand Z, Zarrindast MR, et al. Nicotine improves ethanol-induced memory impairment: the role of dorsal hippocampal NMDA receptors. Life Sci. 2010;86(7-8):260-6.
Rezayof, A., Shirazi-Zand, Z., Zarrindast, M. R., & Nayer-Nouri, T. (2010). Nicotine improves ethanol-induced memory impairment: the role of dorsal hippocampal NMDA receptors. Life Sciences, 86(7-8), 260-6. https://doi.org/10.1016/j.lfs.2009.12.008
Rezayof A, et al. Nicotine Improves Ethanol-induced Memory Impairment: the Role of Dorsal Hippocampal NMDA Receptors. Life Sci. 2010 Feb 13;86(7-8):260-6. PubMed PMID: 20035769.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Nicotine improves ethanol-induced memory impairment: the role of dorsal hippocampal NMDA receptors. AU - Rezayof,Ameneh, AU - Shirazi-Zand,Zahra, AU - Zarrindast,Mohammad-Reza, AU - Nayer-Nouri,Touraj, Y1 - 2009/12/24/ PY - 2009/06/11/received PY - 2009/10/29/revised PY - 2009/12/17/accepted PY - 2009/12/29/entrez PY - 2009/12/29/pubmed PY - 2010/3/10/medline SP - 260 EP - 6 JF - Life sciences JO - Life Sci VL - 86 IS - 7-8 N2 - AIMS: The current study was undertaken to determine the role of dorsal hippocampal N-methyl-d-aspartate (NMDA) receptors in nicotine's effect on impairment of memory by ethanol. MAIN METHODS: Adult male mice were cannulated in the CA1 regions of dorsal hippocampi and trained on a passive avoidance learning task for memory assessment. KEY FINDINGS: We found that pre-training intraperitoneal (i.p.) administration of ethanol (0.5 and 1g/kg) decreased memory retrieval when tested 24h later. Pre-test administration of ethanol reversed the decrease in inhibitory avoidance response induced by pre-training ethanol. Similar to ethanol, pre-test administration of nicotine (0.125-0.75 mg/kg, s.c.) prevented impairment of memory by pre-training ethanol. In the animals that received ethanol (1g/kg, i.p) before training and tested following intra-CA1 administration of different doses of NMDA (0.0005-0.005 microg/mouse), no significant change was observed in the retrieval latencies. Co-administration of the same doses of NMDA with an ineffective dose of nicotine (0.125 mg/kg, s.c.) significantly improved the memory retrieval and mimicked the effects of pre-test administration of a higher dose of nicotine. Pre-test intra-CA1 microinjection of MK-801 (0.25-1 microg/mouse), which had no effect alone, in combination with an effective dose of nicotine (0.75 mg/kg, s.c.) prevented the improving effect of nicotine on memory impaired by pre-training ethanol. Moreover, intra-CA1 microinjection of MK-801 reversed the NMDA-induced potentiation of the nicotine response. SIGNIFICANCE: The results suggest the importance of NMDA glutamate system(s) in the CA1 regions of dorsal hippocampus for improving the effect of nicotine on the ethanol-induced amnesia. SN - 1879-0631 UR - https://www.unboundmedicine.com/medline/citation/20035769/Nicotine_improves_ethanol_induced_memory_impairment:_the_role_of_dorsal_hippocampal_NMDA_receptors_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0024-3205(09)00508-6 DB - PRIME DP - Unbound Medicine ER -