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While evidence from mouse models strongly suggests that prenatal nicotine exposure supports a hyperactive-inattentive phenotype following direct exposure in utero via maternal circulation (Zhu et al 2014), there is little evidence that suggests consequences resulting from indirect exposure of the offspring through a father's use of tobacco products. In order to address the question of the influence of a father smoking on their offspring, we developed a paternal nicotine exposure mouse model in which adult male mice were exposed to nicotine in their drinking water for 12 consecutive weeks.We found that the offspring of these nicotine exposed male mice displayed deficits in working memory and attention, behavioral phenotypes that have been previously linked to ADHD. These intriguing findings were rationale to hypothesize that the fathers' germ cells may have undergone genetic changes as a result of the nicotine exposure and that these changes in the germ cell DNA were the basis for transmission of an ADHD-like phenotype to the offspring.To address these possibilities, we are performing molecular genetic analysis of germ cells and examining gross morphology of the testes of nicotine-exposed fathers to elucidate mechanisms by which paternal nicotine exposure may cause behavioral changes associated with ADHD in the offspring