Cocaine and amphetamine substantially elevate dopamine levels in several forebrain regions involved in reward processing such as the NAc and PFC [1, 51]. The molecular changes induced by cocaine and amphetamine in brain reward regions are typically studied in rodents using investigator-administered or self-administered drug paradigms. Investigator-administration is a relatively high throughput method used to examine differences caused by acute or chronic drug exposure at varying time points after treatment. Self-administration paradigms, while labor-intensive, are better models of addiction and permit the study of rodents that, like humans, choose to take cocaine or another drug of abuse. Additionally, self-administration permits the study of molecular mechanisms involved in drug relapse. Both of these paradigms have been used to identify transient and long-lasting changes in histone acetylation after cocaine or amphetamine exposure [52–54].
