Roles of a novel molecule 'shati' in the development of methamphetamine-induced dependence

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

The ability of drugs of abuse to cause dependence can be viewed as a form of neural plasticity. Recently, we have demonstrated that tumor necrosis factor-α (TNF-α) increases dopamine uptake and inhibits methamphetamine-induced dependence. Moreover, we have identified a novel molecule 'shati' in the nucleus accumbens of mice treated with methamphetamine using the PCR-select cDNA subtraction method and clarified that it is involved in the development of methamphetamine dependence: Treatment with the shati antisense oligonucleotide (shati-AS), which inhibits the expression of shati mRNA, enhanced the methamphetamine-induced hyperlocomotion, sensitization, and conditioned place preference. Further, blockage of shati mRNA by shati-AS potentiated the methamphetamine-induced increase of dopamine overflow and the methamphetamine-induced decrease in dopamine uptake in the nucleus accumbens. Interestingly, treatment with shati-AS also inhibited expression of TNF-α. Transfection of the vector containing shati cDNA into PC12 cells, dramatically induced the expression of shati and TNF-α mRNA, accelerated dopamine uptake, and inhibited the methamphetamine-induced decrease in dopamine uptake. These effects were blocked by neutralizing TNF-α. These results suggest that the functional roles of shati in methamphetamine-induced behavioral changes are mediated through the induction of TNF-α expression which inhibits the methamphetamine-induced increase of dopamine overflow and decrease in dopamine uptake.

Original languageEnglish
Pages (from-to)104-108
Number of pages5
JournalCurrent Neuropharmacology
Volume9
Issue number1
DOIs
Publication statusPublished - 30-03-2011
Externally publishedYes

Fingerprint

Methamphetamine
Dopamine
Tumor Necrosis Factor-alpha
Antisense Oligonucleotides
Nucleus Accumbens
Messenger RNA
Complementary DNA
Neuronal Plasticity
PC12 Cells
Street Drugs
Transfection
Polymerase Chain Reaction

All Science Journal Classification (ASJC) codes

  • Clinical Neurology
  • Pharmacology (medical)
  • Psychiatry and Mental health
  • Neurology
  • Pharmacology

Cite this

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abstract = "The ability of drugs of abuse to cause dependence can be viewed as a form of neural plasticity. Recently, we have demonstrated that tumor necrosis factor-α (TNF-α) increases dopamine uptake and inhibits methamphetamine-induced dependence. Moreover, we have identified a novel molecule 'shati' in the nucleus accumbens of mice treated with methamphetamine using the PCR-select cDNA subtraction method and clarified that it is involved in the development of methamphetamine dependence: Treatment with the shati antisense oligonucleotide (shati-AS), which inhibits the expression of shati mRNA, enhanced the methamphetamine-induced hyperlocomotion, sensitization, and conditioned place preference. Further, blockage of shati mRNA by shati-AS potentiated the methamphetamine-induced increase of dopamine overflow and the methamphetamine-induced decrease in dopamine uptake in the nucleus accumbens. Interestingly, treatment with shati-AS also inhibited expression of TNF-α. Transfection of the vector containing shati cDNA into PC12 cells, dramatically induced the expression of shati and TNF-α mRNA, accelerated dopamine uptake, and inhibited the methamphetamine-induced decrease in dopamine uptake. These effects were blocked by neutralizing TNF-α. These results suggest that the functional roles of shati in methamphetamine-induced behavioral changes are mediated through the induction of TNF-α expression which inhibits the methamphetamine-induced increase of dopamine overflow and decrease in dopamine uptake.",
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Roles of a novel molecule 'shati' in the development of methamphetamine-induced dependence. / Niwa, Minae; Nabeshima, Toshitaka.

In: Current Neuropharmacology, Vol. 9, No. 1, 30.03.2011, p. 104-108.

Research output: Contribution to journalArticle

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