Clearly, cellular and molecular changes of neural adaptation in addiction occur in a substance-specific fashion as well as through common transduction in neurotransmission pathways. Substance-specific effects are not only due to the direct action of certain drugs of abuse on specific receptors, but also by distinctive molecular and cellular changes related to the drugs that may be related to distinctive signaling mechanisms or differences in the modulation of specific neurons and circuits. Using microarray gene expression profiling, Bannon and colleagues (Albertson et al., 2006) observed decreased expression of many genes involved in presynaptic release of neurotransmitter in the NAc of chronic heroin abusers, but not in chronic cocaine abusers. Similarly, the prominent depressed expression of myelin-related genes found in cocaine abusers was not observed in heroin abusers. Their results suggested the divergent effects of cocaine and heroin on gene expression in the NAc, despite their common effects on dopaminergic transmission. Another study by Marie-Claire et al. (2007) also reported differential effects of cocaine and 3,4-methylenedioxymethamphetamine on expression of the Rnd gene family involved in actin cytoskeleton regulation in mouse striatum and noted that the two drugs might act through distinctive pathways to regulate these genes.
