et al., 2010; Thapar et al., 2007; Thapar et al., 2009). In their manuscript, Paz and colleagues used a self-administered maternal nicotine consumption model to assess how prenatal nicotine exposure might influence a variety of neuropsychiatric disorders in mice (Paz, et al., 2007). They found that prenatal nicotine exposure had a significant effect on increasing latency to escape in a learned helplessness paradigm, the degree of spontaneous locomotion, and an increase in addictive behavior as assessed by preference for a place previously associated with cocaine. Paz and colleagues’ findings suggest that prenatal nicotine exposure may be significantly influencing the increased prevalence of MDD, ADHD, and substance abuse found in children and adolescents whose mothers smoked cigarettes during pregnancy, a finding which underscores the behavioral teratogenic effects of maternal cigarette smoking during pregnancy. Moreover, they speculate that this may be due to direct interaction between nicotine and acetylcholine nicotine receptors in the fetal brain. Variations in the genes coding for such receptors may indeed affect the entire biological pathway from prenatal exposure to later development.
