Neonatal ethanol and nicotine exposure causes locomotor activity changes in preweanling animals

Gilbertson, Rebecca; Barron, Susan

doi:10.1016/j.pbb.2005.02.002

Cited by 33 publications

(34 citation statements)

References 68 publications

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“…As for ethanol, according to previous studies in adolescent rodents, even the moderate doses used in the present study result in blood levels well above the legal driving limit (Silveri and Spear, 2000). Ethanol plasma levels are reduced among animals that are simultaneously exposed to ethanol and nicotine (Chen and Harle, 2005;Gilbertson and Barron, 2005;Nowak et al, 1987;Scott et al, 1993). Accordingly, it may be suggested that the less-thanadditive effects of the combined exposure to nicotine and ethanol described in the present study could be due to a reduction in ethanol plasma levels.…”

Section: Methodological Issuessupporting

confidence: 70%

“…However, our results further indicate that the anxiolytic effects of ethanol were reduced by co-exposure with nicotine during adolescence. In light of previous studies on ethanol-nicotine interactions in adult rodents suggesting additive or synergistic anxiolytic effects (depending on the genotype) (Cao et al, 1993); and of contrasting little evidence of interactive effects of nicotine and ethanol during the second postnatal week (Gilbertson and Barron, 2005), our findings provide evidence for adolescence as a critical window for nicotine and ethanol interactions, with unique effects when compared to adulthood and prepubertal periods. More to the point, adolescent nicotine exposure seems to countermand the anxiolytic effect of ethanol consumption.…”

Section: Anxiolytic Effects During Adolescent Exposuresupporting

confidence: 66%

“…Accordingly, it may be suggested that the less-thanadditive effects of the combined exposure to nicotine and ethanol described in the present study could be due to a reduction in ethanol plasma levels. However, this reduction was only described in animals that received oral ethanol, which led to the suggestion that it is related to a nicotineinduced delay in gastric emptying (Chen and Harle, 2005;Gilbertson and Barron, 2005;Nowak et al, 1987;Scott et al, 1993), causing an increased ethanol metabolization by the gastric alcohol dehydrogenase (Oneta et al, 1998). In fact, other studies indicated that chronic nicotine does not change ethanol concentration if ethanol is infused intravenously (Hisaoka and Levy, 1985).…”

Section: Methodological Issuesmentioning

confidence: 99%

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Combined Exposure to Nicotine and Ethanol in Adolescent Mice Differentially Affects Anxiety Levels during Exposure, Short-Term, and Long-Term Withdrawal

Abreu‐Villaça

Nunes

Queiroz-Gomes

et al. 2007

Neuropsychopharmacol

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Smoking and consumption of alcoholic beverages are frequently associated during adolescence. This association could be explained by the cumulative behavioral effects of nicotine and ethanol, particularly those related to anxiety levels. However, despite epidemiological findings, there have been few animal studies of the basic neurobiology of the combined exposure in the adolescent brain. In the present work we assessed, through the use of the elevated plus maze, the short-and long-term anxiety effects of nicotine (NIC) and/or ethanol (ETOH) exposure during adolescence (from the 30th to the 45th postnatal day) in four groups of male and female C57BL/6 mice: (1) Concomitant NIC (nicotine free-base solution (50 mg/ml) in 2% saccharin to drink) and ETOH (ethanol solution (25%, 2 g/kg) i.p. injected every other day) exposure; (2) NIC exposure; (3) ETOH exposure; (4) Vehicle. C57BL/6 mice were selected, in spite of the fact that they present slower ethanol metabolism, because they readily consume nicotine in the concentration used in the present study. During exposure (45th postnatal day: PN45), our results indicated that ethanol was anxiolytic in adolescent mice and that nicotine reverted this effect. Short-term drug withdrawal (PN50) elicited sex-dependent effects: exposure to nicotine and/or ethanol was anxiogenic only for females. Although neither nicotine nor ethanol effects persisted up to 1 month postexposure (PN75), the coadministration elicited an anxiogenic response. In spite of the fact that generalizations based on the results from a single strain of mice are prone to shortcomings, our results suggest that the deficient response to the anxiolytic effects of ethanol in adolescents co-exposed to nicotine may drive higher ethanol consumption. Additionally, increased anxiety during long-term smoking and drinking withdrawal may facilitate relapse to drug use.

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Section: Methodological Issuessupporting

confidence: 70%

Section: Anxiolytic Effects During Adolescent Exposuresupporting

confidence: 66%

Section: Methodological Issuesmentioning

confidence: 99%

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Combined Exposure to Nicotine and Ethanol in Adolescent Mice Differentially Affects Anxiety Levels during Exposure, Short-Term, and Long-Term Withdrawal

Abreu‐Villaça

Nunes

Queiroz-Gomes

et al. 2007

Neuropsychopharmacol

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“…prenatal exposure to 2 mg kg −1 day −1 nicotine via osmotic minipump (Lichtensteiger et al 1988;Navarro et al 1989;Shacka et al 1997), with contradictory reports regarding normal or retarded Bwt gain after postnatal exposure to 6-12 mg kg −1 day −1 nicotine (Gilbertson and Barron 2005;Narayanan et al 2002;Vaglenova et al 2004). Similarly, there are contradictory reports on pup Bwt gain after prenatal or postnatal exposure to 4-5 g/kg EtOH gavage (Gilbertson and Barron 2005;Iqbal et al 2004).…”

Section: Resultsmentioning

confidence: 99%

“…Similarly, there are contradictory reports on pup Bwt gain after prenatal or postnatal exposure to 4-5 g/kg EtOH gavage (Gilbertson and Barron 2005;Iqbal et al 2004). These differences may be strain-or gender-dependent or attributable to technical variances.…”

Section: Resultsmentioning

confidence: 99%