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Related Experiment Videos

Effect of flunarizine and nimodipine on the decrease in tryptophan hydroxylase activity induced by methamphetamine

M Johnson1, K Mitros, D M Stone

  • 1Department of Pharmacology and Toxicology, University of Utah, Salt Lake City.

The Journal of Pharmacology and Experimental Therapeutics
|May 1, 1992
PubMed
Summary

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Calcium channel blockers like flunarizine may protect against MDMA-induced serotonin depletion by affecting calcium influx. However, the mechanisms by which MDMA and METH reduce tryptophan hydroxylase activity differ.

Area of Science:

  • Neuropharmacology
  • Neurochemistry
  • Toxicology

Background:

  • Repeated high doses of methamphetamine (METH) and 3,4-methylenedioxymethamphetamine (MDMA) can decrease central serotonin (5-HT) levels and tryptophan hydroxylase (TPH) activity.
  • Calcium influx is a potential factor in neurochemical alterations induced by psychoactive substances.

Purpose of the Study:

  • To evaluate the effect of calcium channel blockers (CCBs) on METH- and MDMA-induced reductions in central TPH activity and 5-HT concentration.
  • To investigate the potential role of calcium influx in the neurotoxic effects of METH and MDMA.

Main Methods:

  • Rats were administered repeated high doses of METH or MDMA.
  • Rats were treated with CCBs (flunarizine, nimodipine, diltiazem, TA-3090) or haloperidol.
  • TPH activity and 5-HT/5-hydroxyindoleacetic acid concentrations in cortical and neostriatal tissues were measured.

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Main Results:

  • Flunarizine prevented the decline in TPH activity and 5-HT levels induced by MDMA, but not METH.
  • Other CCBs and haloperidol did not show protective effects against METH or MDMA.
  • Flunarizine's protective action was not mediated by dopamine D-2 receptor blockade.

Conclusions:

  • Calcium influx may play a role in the MDMA-induced decrease in central TPH activity.
  • The neurochemical mechanisms underlying the TPH-inhibitory effects of METH and MDMA appear to be distinct.