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SPECIAL ISSUE: PSYCHOPHARMACOLOGY AND PSYCHOSOMATIC RESEARCH |
From the Behavioral Neuroscience Program, Department of Psychology, State University of New York at Buffalo (G.T.), and Department of Social Sciences, Medaille College (J.M.H.), Buffalo, NY.
Address reprint requests to: German Torres, PhD, Behavioral Neuroscience Program, Department of Psychology, State University of New York at Buffalo, Buffalo, NY 14260. Email: gtorres{at}acsu.buffalo.edu
Addictive drugs like cocaine, ethanol, and morphine activate signal transduction pathways that regulate brain gene expression. Such regulation is modulated by the presence of certain transcription factor proteins present in a given neuron. This article summarizes the effects of several addictive drugs on transcriptional processes contributing to the development of a drug-dependent state. The characterization of drug-induced changes in gene expression shows promise for improving our understanding of drug-addiction phenomena and cellular modes of cocaine, ethanol, and morphine action.
Key Words: addiction dopamine genes mutagenesis rodents striatum
Abbreviations: ACTH = adrenocorticotropin hormone; cAMP = cyclicadenosine monophosphate; CART = cocaine- and amphetamine-regulatedtranscript; CBP = CREB-binding protein; CRE = cAMP-regulatedenhancer; CREB = cAMP response-element binding protein; CRF =corticotropin-releasing factor; DA = dopamine; FRAs =Fos-related antigens; G-proteins = guaninenucleotidebinding proteins; GABA =
-aminobutyric acid; IEG = immediate-early gene; JAK2-STAT = Janus kinasesignaltransducer and activator of transcription; LC = locus ceruleus; NE = norepinephrine; NGFI = nerve growth factor I; NMDA= N-methyl-D-aspartate; PKA = proteinkinase A; PVh = paraventricular nucleus of thehypothalamus; 5-HT = 5-hydroxytryptamine; SN = substantianigra; THP = tetrahydropapaveroline; VMAT2 = vesicularmonoamine transporter 2; VTA = ventral tegmental area.
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