Abstract
Experience with amphetamine-like psychostimulants, such as amphetamine, methamphetamine (MAP) or cocaine, results in enhanced neuronal and behavioral responses to subsequent drug exposure. This behavioral sensitization, which is believed to be a part of the mechanisms sustaining drug addiction and drug-induced psychosis in human beings1, is a long-lasting adaptation to drugs of abuse based on persistent cellular and neurochemical changes in some specific brain circuits including the ventral tegmental area (VTA), nucleus accumbens (NAc) and cerebral cortex2. This type of brain plasticity seems to require the gene expression that drives the cascade leading to the establishment and maintenance of the sensitized behavioral responsiveness to stimulants or stress because the application of protein synthesis inhibitors blocks the induction of the sensitization3. Therefore, identification of the stimulant-responsive gene expression that is specifically observed under sensitization-inducing conditions affords helpful clues to understanding the molecular and neuronal mechanism of this unique behavioral plasticity.
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Kajii, Y., Hashimoto, T., Umino, A., Nishikawa, T. (2002). Neocortical Gene Expression Associated with Behavioral Sensitization to Psychostimulants. In: Nagatsu, T., Nabeshima, T., McCarty, R., Goldstein, D.S. (eds) Catecholamine Research. Advances in Behavioral Biology, vol 53. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-3538-3_96
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DOI: https://doi.org/10.1007/978-1-4757-3538-3_96
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