Abstract
Cocaine modulates the expression of several transcription factors (TFs) by altering their transcriptional level, translocation to the nucleus, or promoting their binding to the DNA. The effect is specific of certain brain areas, and depends on the length of the treatment, route of administration, and experimental approach. The TFs affected by cocaine can be classified in: (1) TFs directly regulated by cocaine, namely CREB and FOS/JUN (AP-1). The truncated isoform ΔFOSB plays a key role in gene regulation related to neural plasticity; (2) immediate early genes located downstream of CREB and/or AP-1 and which regulate the expression of late-response genes involved in cellular responses; (3) homeogenes; (4) TFs involved in dopaminergic differentiation; and (5) TFs related to circadian rhythm. These TFs control the transcriptional activity of many target genes related to neural plasticity and which induce the long-term changes triggered by cocaine. Conversely, TFs also regulate the rewarding properties of cocaine and its addictive potential.
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