Research using animal models has documented plausible neural pathways through which prenatal exposure to cigarettes, alcohol, and other drugs could cause offspring substance use and abuse. Animals prenatally exposed to alcohol show greater preference for alcohol and consume significantly more alcohol than unexposed controls (Spear and Molina, 2005), and animals prenatally exposed to nicotine show long-term alterations in the density of nicotinic acetylcholine receptors and demonstrate increased nicotine self-administration (Slotkin, 2008). These prenatal exposures are also associated with morphological and neurochemical alterations of midbrain areas mediating reward, indicating that the reward system and reward-driven behaviors may be altered by intrauterine exposure in ways that predispose animals to increased self-administration of drugs (Lidow, 2003, Malanga and Kosofsky, 2003). These studies provide evidence that prenatal drug exposure, independent of familial behavioral and environmental factors, can result in increased behavior related to drug reinforcement.
