Preclinical data elucidate molecular and neural mechanisms of perinatal nicotine effects on neurodevelopment and behavior: translational opportunities and implications.

Department of Psychiatry, University of Pennsylvania, Philadelphia, PA 19104, USA.
Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology (Impact Factor: 7.05). 11/2010; 35(12):2322-3. DOI: 10.1038/npp.2010.147
Source: PubMed
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    • "Nicotine, among the inhaled ingredients of tobacco smoke, is thought as the main disruptor of the functional development of fetal brain (Pauly and Slotkin 2008). Reports from animal models also indicate that gestational nicotine exposure (GNE) disrupts development of critical neural pathways in the developing brain and leads to neurobehavioral impairments in the offspring (Lerman 2010; Pauly and Slotkin 2008; Slotkin 1998). "
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    ABSTRACT: Gestational nicotine exposure is associated with cognitive abnormalities in young offspring. However, practical strategies for prevention or treatment of impaired cognitive behaviors of offspring are not available due to the lack of systematic investigation of underlying mechanism. Therefore, this study aimed at examining the effects of gestational and/or perinatal nicotine exposure (GPNE) on cognitive behaviors in offspring of C57BL/6J mice to provide systematic behavioral data. Pregnant mice were exposed to nicotine via sweetened drinking water during six time-windows, including gestational day 0 to day 13 (G0-G13), G14-postnatal day 0 (P0), G0-P0, G14-P7, G0-P7, and P0-P7. During P42-P56 days, both male and female offspring were given a battery of behavioral tests. Depending on the time of exposure, GPNE impaired working memory, object-based attention, and prepulse inhibition in male and female offspring to different extents. Nicotine exposure during G14-P0 also decreased norepinephrine turnover in the prefrontal cortex on P28 and P56. Overall results indicate that nicotine exposure during any time-windows of development impairs cognitive behaviors in offspring, and suggest that certain time-windows, e.g., G14-P0, should be selected for further studies on the underlying neurochemical or molecular mechanisms.
    Psychopharmacology 06/2013; 230(3). DOI:10.1007/s00213-013-3175-9 · 3.88 Impact Factor
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    ABSTRACT: Despite progress made in the treatment of tobacco dependence, currently available treatments are effective for only a fraction of smokers. The aim of this study was to evaluate the association between the effectiveness of treatment with nicotine or bupropion in heavy smokers (n=70), and 6 candidate polymorphisms in CYP2A6, 5-HTT and HTR2A genes. Analysis revealed a significant association between "favourable" genotype combination carriers (CYP2A6 "slow metabolizer" or 5HTT L-allele or HTR2A-1438GG) and nicotine treatment outcome (OR=2.69, 95% CI=1.28-5.64). Genetic variations in CYP2A6 gene or genotypes associated with reduced synaptic serotonin activity may influence the success of smoking cessation treatment.
    Pharmacopsychiatry 10/2013; 47(1). DOI:10.1055/s-0033-1358393 · 1.85 Impact Factor


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