Reduction of rat striatal thyrotropin-releasing hormone receptors produced by repeated methamphetamine administration

Nakashima, Makoto; Kajita, Saburo; Otsuki, Saburo

doi:10.1016/0006-3223(89)90163-7

Cited by 2 publications

(1 citation statement)

References 21 publications

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“…Various neurochemical adaptations have been found in the sensitization phenomenon, including up‐ or down‐regulation of D1 dopamine,6 sigma,7–9 and neuropeptide receptors,10–12 altered dopamine transporters mRNA,13 changes in the alpha and beta subunits of trimeric G proteins14–16 and enzymes for dopamine synthesis and metabolism,2 increased adenylyl cyclase activity, cyclic AMP and protein kinase A,17 increased calmodulin and activated CamK II,18–20 and increased c‐fos and AP‐1 binding protein 21,22. However, since these subcellular neurochemical adaptations are all transient or reversible, they must be converted to more lasting plastic brain changes during sensitization.…”

Section: Introductionmentioning

confidence: 99%

Gene Expression Related to Synaptogenesis, Neuritogenesis, and MAP Kinase in Behavioral Sensitization to Psychostimulants

Ujike

Takaki

Kodama

et al. 2002

Annals of the New York Academy of Sciences

116

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The most important characteristic of behavioral sensitization to psychostimulants, such as amphetamine and cocaine, is the very long‐lasting hypersensitivity to the drug after cessation of exposure. Rearrangement and structural modification of neural networks in CNS must be involved in behavioral sensitization. Previous microscopic studies have shown that the length of dendrites and density of dendritic spines increased in the nucleus accumbens and frontal cortex after repeated exposure to amphetamine and cocaine, but the molecular mechanisms responsible are not well understood. We investigated a set of genes related to synaptogenesis, neuritogenesis, and mitogen‐activated protein (MAP) kinase after exposure to methamphetamine. Synaptophysin mRNA, but not VAMP2 (synaptobrevin 2) mRNA, which are considered as synaptogenesis markers, increased in the accumbens, striatum, hippocampus, and several cortices, including the medial frontal cortex, after a single dose of 4 mg/kg methamphetamine. Stathmin mRNA, but not neuritin or narp mRNA, which are markers for neuritic sprouting, increased in the striatum, hippocampus, and cortices after a single dose of methamphetamine. The mRNA of arc, an activity‐regulated protein associated with cytoskeleton, but not of alpha‐tubulin, as markers for neuritic elongation, showed robust increases in the striatum, hippocampus, and cortices after a single dose of methamphetamine. The mRNAs of MAP kinase phosphatase‐1 (MKP‐1), MKP‐3, and rheb, a ras homologue abundant in brain, were investigated to assess the MAP kinase cascades. MKP‐1 and MKP‐3 mRNAs, but not rheb mRNA, increased in the striatum, thalamus, and cortices, and in the striatum, hippocampus, and cortices, respectively, after a single methamphetamine. Synaptophysin and stathmin mRNAs did not increase again after chronic methamphetamine administration, whereas the increases in arc, MKP‐1, and MKP‐3 mRNAs persisted in the brain regions after chronic methamphetamine administration. These findings indicate that the earlier induction process in behavioral sensitization may require various plastic modifications, such as synaptogenesis, neuritic sprouting, neuritic elongation, and activation of MAP kinase cascades, throughout almost the entire brain. In contrast, later maintenance process of sensitization may require only limited plastic modification in restricted regions.

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