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; in turn, early stress may produce precocious maturation of the prefrontal cortex, leading to its under-development (Teicher et al., 2002). This process and addiction itself are manifestations of brain plasticity that appear to operate with the same neuroanatomical mechanisms and systems. Notably, parental SUD has a positive dose–effect relationship with the rate of pubertal maturation in boys, related in turn with their behavioral dysregulation (Kirillova et al., 2001, 2008). Inasmuch as the familiality of both SUD liability and behavioral dysregulation is largely due to heritability rather than common environment, these data suggest that genetic mechanisms of neural maturation and plasticity are involved in the transmission of addiction liability.
