Substance use disorders are neuropsychiatric illnesses that have substantial negative
biopsychosocial impact. These diseases are defined as compulsive abuse of licit or illicit substances
despite adverse medicolegal consequences. Although much research has been conducted to elucidate
the pathobiological bases of these disorders, much remains to be done to develop an overarching
neurobiological understanding that might be translatable to beneficial pharmacological therapies.
Recent advances in epigenetics promise to lead to such an elucidation. Here I provide a brief
overview of observations obtained using some models of psychostimulant administration in rodents.
The review identifies CREB binding protein (CBP), HDAC1, HDAC2, HADC3, HDAC4, and HDAC5 as important
players in the acetylation and deacetylation processes that occur after contingent or non-contingent administration of
psychostimulants. These observations are discussed within a framework that suggests a need for better animal models of
addiction in order to bring these epigenetic advances to bear on the pharmacological treatment of human addicts.
Keywords: Acetylation, addiction, cocaine, dorsal striatum, epigenetics, gene expression, methamphetamine, nucleus
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