3,4-methylenedioxymethamphetamine ('Ecstasy') promotes the translocation of protein kinase C (PKC): requirement of viable serotonin nerve terminals

H. Kenneth Kramer, Jose C P Poblete, Efrain C. Azmitia

Research output: Contribution to journalArticlepeer-review


The metabolic effects of the neurotoxic, ring-substituted amphetamine 3,4-methylenedioxy-methamphetamine (MDMA or 'Ecstasy') were examined in vivo. In this study, we focused on the ability of MDMA to induce a translocation of the calcium and phospholipid-dependent protein kinase C (PKC) from cytosol to the cortical plasma membrane. Two injections of MDMA (20 mg/kg; 10 h apart; s.c.) increased the density of membrane bound PKC sites by 48.0% over saline treated animals without mediating a significant change in ligand ([3H]phorbol 12,13 dibutyrate; [3H]PDBu) affinity. Longer drug treatments (8 × 20 mg/kg) induced a lasting (up to 5 days post-treatment) increase in the density of membrane-bound PKC. Prior destruction of cortical 5-HT nerve terminals with p-chloroamphetamine (PCA) prevents this effect and suggests that viable 5-HT uptake sites are essential for MDMA-induced PKC translocation. These results demonstrate that MDMA-induced PKC translocation to mediated by viable cortical 5-HT nerve terminals, and that prolonged kinase activation may contribute to MDMA-induced serotonergic neurotoxicity.

Original languageEnglish (US)
Pages (from-to)1-8
Number of pages8
JournalBrain Research
Issue number1-2
StatePublished - May 22 1995


  • Calcium
  • Degeneration
  • Release
  • Second messenger
  • Serotonin
  • Serotonin receptor

ASJC Scopus subject areas

  • General Neuroscience
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology


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