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Methamphetamine-induced rapid decrease in dopamine transporter function: role of dopamine and hyperthermia.

R R Metzger1, H M Haughey, D G Wilkins

  • 1Program in Neuroscience, University of Utah, Salt Lake City, Utah 84112, USA.

The Journal of Pharmacology and Experimental Therapeutics
|November 18, 2000
PubMed
Summary
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Repeated methamphetamine (METH) use significantly impairs dopamine transporter (DAT) function, influenced by hyperthermia and dopamine levels. Single METH doses do not show these effects, suggesting distinct mechanisms for acute versus chronic METH toxicity.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Toxicology

Background:

  • Methamphetamine (METH) abuse leads to significant neurotoxicity.
  • Dopamine transporter (DAT) function is crucial for regulating dopamine levels and is a target of METH toxicity.

Purpose of the Study:

  • To investigate the differential effects of single versus multiple high-dose methamphetamine administrations on dopamine transporter (DAT) function.
  • To elucidate the roles of hyperthermia, dopamine (DA), and oxidative stress in METH-induced DAT dysfunction.

Main Methods:

  • Assessing [(3)H]DA uptake in rat striatal synaptosomes after METH administration.
  • Employing interventions to block hyperthermia, deplete DA, or antagonize DA receptors.
  • Utilizing an antioxidant to investigate the role of oxygen radicals.

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Main Results:

  • Multiple METH doses decreased DAT function, an effect attenuated by preventing hyperthermia, depleting DA, or using DA antagonists.
  • Hyperthermia was blocked by DA depletion and antagonists, and its reinstatement partially restored METH-induced DAT decrease.
  • Single METH administration's DAT function decrease was not affected by hyperthermia prevention, DA depletion, or DA antagonists.
  • Antioxidant pretreatment partially prevented DAT function decrease after multiple METH doses, but not after a single dose.

Conclusions:

  • Dopamine, hyperthermia, and oxygen radicals contribute to the rapid decrease in DAT function following multiple METH injections.
  • These factors do not appear to be involved in the DAT function reduction caused by a single METH administration.
  • Distinct mechanisms underlie the neurotoxic effects of single versus repeated high-dose METH exposure on DAT.