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Related Experiment Videos

Dopamine-glutamate interactions in methamphetamine-induced neurotoxicity

J F Marshall1, S J O'Dell, F B Weihmuller

  • 1Department of Psychobiology, University of California, Irvine.

Journal of Neural Transmission. General Section
|January 1, 1993
PubMed
Summary

Repeated methamphetamine (m-AMPH) exposure damages dopamine (DA) terminals. Blocking N-methyl-D-aspartate (NMDA) or dopamine D1/D2 receptors protects against this damage by reducing DA overflow.

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Neurotoxicology

Background:

  • Repeated methamphetamine administration causes dopamine terminal damage.
  • N-methyl-D-aspartate (NMDA) and dopamine receptor antagonists show protective effects.

Purpose of the Study:

  • To investigate the role of dopamine (DA) overflow in methamphetamine-induced neurotoxicity.
  • To determine if NMDA and dopamine receptor antagonists attenuate DA overflow and protect DA terminals.

Main Methods:

  • Rats received repeated methamphetamine (m-AMPH) doses.
  • Striatal microdialysis measured extracellular DA levels.
  • Neuroprotective agents (MK-801, SCH 23390, eticlopride) were coadministered.

Main Results:

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  • Methamphetamine caused a significant and prolonged increase in extracellular DA.
  • NMDA and dopamine receptor antagonists markedly reduced this DA overflow.
  • DA overflow correlated with subsequent DA terminal damage.

Conclusions:

  • Attenuation of methamphetamine-evoked DA overflow by NMDA and dopamine receptor antagonists explains their neuroprotective effects.
  • Elevated extracellular DA concentrations are crucial to methamphetamine's neurotoxic actions.