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Substance Abuse and Addiction 391age. The available evidence suggests that delaying initiation of smoking would increasethe likelihood of success when the smoker later engages in a nicotine dependencetreatment program (Breslau & Peterson, 1996).Genetic factors are thought to play a role in vulnerability to all addictions. Inthe case of nicotine, heredity is estimated to account for 70% of the variance inmoving from initiation of smoking to nicotine addiction (Sullivan & Kendler,1999). Relevant nicotine exposure may be as early as in utero exposure. Womenwhose mothers smoked during pregnancy had a four-fold increase in smoking ratesas adults when compared to women whose mothers did not smoke during theirpregnancy (Kandel, Wu, & Davies, 1994).StimulantsAnimal models of adolescence may shed light on critical periods of drug exposureand the mechanisms by which this exposure could have effects far into thefuture. For example, Mague and colleagues (Mague, Andersen, & Carlezon, 2005)reported that exposure of rat pups to two injections of the stimulant methylphenidateduring preadolescence (postnatal days 20–35, approximating ages 4–12 yearsin humans) resulted in lasting changes in the brain reward system as measured bysensitivity to the rewarding effects of cocaine tested during adulthood. Sensitivitywas measured by changes in the threshold for intracranial self-stimulationproduced by cocaine. The early stimulant exposure rendered the rats less sensitiveto cocaine when they became adults. These findings are an interesting contrastto the opposite finding in adult rats in which stimulant exposure sensitizesthe animal to subsequent doses of stimulant (Meririnne, Kankaanpaa, & Seppala,2001). They may also help to explain the lack of severe problems in babies bornto cocaine using mothers when compared to appropriate controls (Hurt, Brodsky,Roth, Malmud, & Giannetta, 2005).Other studies in animal models have shown that early methylphenidate treatmentalso reduces the effects of cocaine in adulthood as measured by place preference(Carlezon, Mague, & Andersen, 2003). These findings are important becauseof the large number of children who receive methylphenidate as effective treatmentfor attention deficit/hyperactivity disorder (ADHD). Concern has been expressedbecause of the possibility that exposing children to a drug that has amechanism of action similar to cocaine could lead to later stimulant abuse. Actualstudies of children with carefully diagnosed ADHD have found that untreatedADHD is indeed associated with an increased probability of substance abuse, butin those who have been treated with methylphenidate, the risk of substance abuseis significantly lower (Wilens, Faraone, Biederman, & Gunawardene, 2003). Thusthe clinical findings are consistent with the report in adolescent rats showing reducedstimulant effects after adolescent exposure. It should be noted, however,