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Nicotine improves ethanol-induced impairment of memory: possible involvement of nitric oxide in the dorsal hippocampus of mice.
Neuroscience. 2012 Sep 06; 219:82-91.N

Abstract

In the present study, the possible involvement of nitric oxide (NO) systems in the dorsal hippocampus in nicotine's effect on ethanol-induced amnesia and ethanol state-dependent memory was investigated. Adult male mice were cannulated in the CA1 regions of the dorsal hippocampus and trained on a passive avoidance learning task for memory assessment. We found that pre-training intraperitoneal (i.p.) administration of ethanol (1 g/kg) decreased inhibitory avoidance memory when tested 24 h later. The response induced by pre-training ethanol was significantly reversed by pre-test administration of the drug. Similar to ethanol, pre-test administration of nicotine (0.4 and 0.8 μg/mouse, intra-CA1) alone and nicotine (0.2, 0.4 and 0.8 μg/mouse) plus an ineffective dose of ethanol also significantly reversed the amnesia induced by ethanol. Ethanol amnesia was also prevented by pre-test administration of L-arginine (1.2 μg/mouse, intra-CA1), a NO precursor. Interestingly, an ineffective dose of nicotine (0.2 μg/mouse) in combination with a low dose of L-arginine (0.8 μg/mouse) synergistically improved memory performance impaired by ethanol given before training. In contrast, pre-test intra-CA1 microinjection of L-NAME (NG-nitro-L-arginine methyl ester), a nitric oxide synthase (NOS) inhibitor (0.4 and 0.8 μg/mouse), which reduced memory retrieval in inhibitory avoidance task by itself, in combination with an effective dose of nicotine (0.4 μg/mouse) prevented the improving effect of nicotine on memory impaired by pre-training ethanol. Moreover, intra-CA1 microinjection of L-NAME reversed the L-arginine-induced potentiation of the nicotine response. The results suggest the importance of NO system(s) in the CA1 regions of the dorsal hippocampus for improving the effect of nicotine on the ethanol-induced amnesia.

Authors+Show Affiliations

Department of Biology, Faculty of Basic Sciences, Islamic Azad University, Lahijan Branch, Lahijan, Iran. raoufinasrin@yahoo.co.ukNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

22698687

Citation

Raoufi, N, et al. "Nicotine Improves Ethanol-induced Impairment of Memory: Possible Involvement of Nitric Oxide in the Dorsal Hippocampus of Mice." Neuroscience, vol. 219, 2012, pp. 82-91.
Raoufi N, Piri M, Moshfegh A, et al. Nicotine improves ethanol-induced impairment of memory: possible involvement of nitric oxide in the dorsal hippocampus of mice. Neuroscience. 2012;219:82-91.
Raoufi, N., Piri, M., Moshfegh, A., & Shahin, M. S. (2012). Nicotine improves ethanol-induced impairment of memory: possible involvement of nitric oxide in the dorsal hippocampus of mice. Neuroscience, 219, 82-91. https://doi.org/10.1016/j.neuroscience.2012.06.003
Raoufi N, et al. Nicotine Improves Ethanol-induced Impairment of Memory: Possible Involvement of Nitric Oxide in the Dorsal Hippocampus of Mice. Neuroscience. 2012 Sep 6;219:82-91. PubMed PMID: 22698687.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Nicotine improves ethanol-induced impairment of memory: possible involvement of nitric oxide in the dorsal hippocampus of mice. AU - Raoufi,N, AU - Piri,M, AU - Moshfegh,A, AU - Shahin,M-S, Y1 - 2012/06/12/ PY - 2012/04/09/received PY - 2012/06/02/revised PY - 2012/06/04/accepted PY - 2012/6/16/entrez PY - 2012/6/16/pubmed PY - 2012/12/10/medline SP - 82 EP - 91 JF - Neuroscience JO - Neuroscience VL - 219 N2 - In the present study, the possible involvement of nitric oxide (NO) systems in the dorsal hippocampus in nicotine's effect on ethanol-induced amnesia and ethanol state-dependent memory was investigated. Adult male mice were cannulated in the CA1 regions of the dorsal hippocampus and trained on a passive avoidance learning task for memory assessment. We found that pre-training intraperitoneal (i.p.) administration of ethanol (1 g/kg) decreased inhibitory avoidance memory when tested 24 h later. The response induced by pre-training ethanol was significantly reversed by pre-test administration of the drug. Similar to ethanol, pre-test administration of nicotine (0.4 and 0.8 μg/mouse, intra-CA1) alone and nicotine (0.2, 0.4 and 0.8 μg/mouse) plus an ineffective dose of ethanol also significantly reversed the amnesia induced by ethanol. Ethanol amnesia was also prevented by pre-test administration of L-arginine (1.2 μg/mouse, intra-CA1), a NO precursor. Interestingly, an ineffective dose of nicotine (0.2 μg/mouse) in combination with a low dose of L-arginine (0.8 μg/mouse) synergistically improved memory performance impaired by ethanol given before training. In contrast, pre-test intra-CA1 microinjection of L-NAME (NG-nitro-L-arginine methyl ester), a nitric oxide synthase (NOS) inhibitor (0.4 and 0.8 μg/mouse), which reduced memory retrieval in inhibitory avoidance task by itself, in combination with an effective dose of nicotine (0.4 μg/mouse) prevented the improving effect of nicotine on memory impaired by pre-training ethanol. Moreover, intra-CA1 microinjection of L-NAME reversed the L-arginine-induced potentiation of the nicotine response. The results suggest the importance of NO system(s) in the CA1 regions of the dorsal hippocampus for improving the effect of nicotine on the ethanol-induced amnesia. SN - 1873-7544 UR - https://www.unboundmedicine.com/medline/citation/22698687/Nicotine_improves_ethanol_induced_impairment_of_memory:_possible_involvement_of_nitric_oxide_in_the_dorsal_hippocampus_of_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0306-4522(12)00602-1 DB - PRIME DP - Unbound Medicine ER -