Such individual characteristics – potential sources of common variance between liabilities to specific addictions as well as between these liabilities and other behavioral traits – have been recorded at all levels of biological organization. In particular, psychophysiological correlates of disruptive behavior disorders (attention deficit hyperactivity and conduct disorders) and SUD are consistent with deviations in frontal and prefrontal brain maturation (Bauer and Hesselbrock, 2003). Importantly, these brain areas are involved in both behavior regulation and reward, including drug-related reinforcement. The density of dopaminergic, adrenergic, serotonergic, cholinergic, and GABAergic receptors, all involved in response to psychoactive drugs, parallels synaptogenesis (Lidow et al., 1991). Overproduction and subsequent pruning of synaptic contacts are characteristic of the peripubertal period, when the risk for non-normative behavior is maximized. Pubertal maturation rate influences neurodevelopment, with these ontogenetic changes reflected in mental processes germane to cognition, affect, and behavior regulation (Teicher et al., 2003), and thus to the ontogenesis of the SUD liability phenotype. Variation (including sex differences) in the rate of neuronal pruning in adolescence, particularly dopamine neurons in striatum, has behavioral and stress reactivity consequences;
