In the past decade, global analysis of gene expression using high-throughput microarrays and, more recently, the use of genomic sequencing, have been frequently applied to the problem of addiction (Hitzemann et al., 2013) and have shed new light on molecular pathways that are altered in the addicted brain. These studies have been conducted in diverse contexts including rodents, nonhuman primates, and postmortem human brain samples and have revealed some important divergences. The differences in what is observed appear to be mainly due to timing and exposure: each study is a snapshot of the addicted brain in dynamic processes. In rodents, some studies have profiled gene expression during drug-self administration, whereas others during withdrawal. An important distinction between the rodent models and human postmortem brain is that in rodents, “chronic exposure” usually refers to a few days or weeks, whereas in humans, it usually denotes many years of heavy use. This one fact appears to explain most of the differences observed in studies of rodents versus those on people. More widespread and divergent molecular and cellular changes have been observed in
