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| Research article summary (published 29 Jun 2009): |
Increased apoptosis and reduced neuronal and glial densities in the hippocampus due to nicotine and ethanol exposure in adolescent mice.
Full Abstract
It has been recently shown that nicotine and ethanol interact during adolescence affecting memory/learning and anxiety levels. Considering the role of the hippocampus in both anxiety and memory/learning, we investigated whether adolescent nicotine and/or ethanol administration elicit apoptotic cell death and whether this results in neuronal and/or glial density alterations in the following regions of the hippocampus: granular layer of the dentate gyrus (GrDG), molecular layer (Mol), CA1, CA2 and CA3. From the 30th to the 45th postnatal day, C57BL/6 male and female mice were exposed to nicotine free base (NIC) and/or ethanol (ETOH). Four groups were analyzed: (1) concomitant NIC (50mug/ml in 2% saccharin to drink) and ETOH (25%, 2g/kg i.p. injected every other day) exposure; (2) NIC exposure; (3) ETOH exposure; (4) vehicle. We evaluated cell degeneration (TUNEL assay), neuronal and glial densities (optical disector) and region thicknesses at the end of the period of exposure. Our results demonstrate that ETOH elicited an increase in TUNEL-positive cells relative to the vehicle group in all hippocampal regions. NIC elicited less severe region-dependent effects: the number of TUNEL-positive cells was significantly increased in the Mol and CA1 when compared to the vehicle group. These results were paralleled by reductions in neuronal and glial cells densities, which indicate that both cell types are sensitive to the neurotoxic effects of these drugs. There were no effects on region thicknesses. On the other hand, concomitant NIC and ETOH reduced the adverse effects of the drugs when administered separately. This ability of nicotine and ethanol co-exposure to lessen the adverse effects of nicotine and ethanol may contribute to adolescents co-use and co-abuse of tobacco and alcoholic beverages.
Author information
Author/s: Oliveira-da-Silva, Andreia (A); Vieira, Fernanda B (FB); Cristina-Rodrigues, Fabiana (F); Filgueiras, Cláudio C (CC); Manhães, Alex C (AC); Abreu-Villaça, Yael (Y);
Affiliation: Laboratório de Neurofisiologia, Departamento de Ciências Fisiológicas, Instituto de Biologia Roberto Alcantara Gomes, Centro Biomédico, Universidade do Estado do Rio de Janeiro, Av. Prof. Manoel de Abreu 444, 5 andar, Vila Isabel, Rio de Janeiro, RJ 20550-170, Brazil.
Journal and publication information
Publication Type: Journal Article; Research Support, Non-U.S. Gov't
Journal: International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience (Int J Dev Neurosci), published in England. (Language: eng)
Reference: 2009-Oct; vol 27 (issue 6) : pp 539-48
Dates: Created 2009/08/18; Completed 2009/11/13;
PMID: 19576279, status: MEDLINE (last retrieved date: 11/15/2009)
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
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Associated Chemicals: Central Nervous System Depressants (0) ; Nicotinic Agonists (0) ; Nicotine (54-11-5) ; Ethanol (64-17-5)Related articles
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