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.

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Ethanol exposure during development promotes a series of neurobehavioral disorders in both humans and rodents. While in humans the deficits are most evident during childhood, in rodents most studies focus on the investigation of effects from adolescence onward. Considering that the examination of habituation at early ages provides a useful tool to assess learning and memory and its development, here we used the tail suspension test (TST) to investigate whether habituation of infant and adolescent mice is affected by ethanol exposure during the neonatal period. From postnatal day (PN) 2 to PN6, Swiss mice either received ethanol (5g/kg ip, ETOH) or saline (CONT) every other day. Mice were subjected to the TST for 6 min on alternate days from PN14 to PN20 (infancy) or from PN28 to PN34 (early adolescence). Only lateral (left- or rightward) movements with the torso were scored and used as a measure of activity. Differences between ETOH and CONT groups were observed during infancy. The activity decreased from PN16 to PN20 in the CONT group but did not change in the ETOH group. In addition, the averaged activity of the ETOH group was higher than that of the CONT group. No differences were observed between CONT and ETOH mice tested from PN28 to PN34. Our data suggest that the TST can be an important tool for the study of the effects of neonatal ethanol exposure in infant mice.