Potentiation of (DL)-3,4-methylenedioxymethamphetamine (MDMA)-induced toxicity by the serotonin 2A receptior partial agonist d-lysergic acid diethylamide (LSD), and the protection of same by the serotonin 2A/2C receptor antagonist MDL 11,939

  1. Brian D. Armstrong1,*,
  2. Elena Paik1,
  3. Seririthanar Chhith1,
  4. Vincent Lelievre1,
  5. James A. Waschek1,
  6. Sherrel G. Howard2

Article first published online: 26 OCT 2004

DOI: 10.1002/nrc.20023

Issue

Neuroscience Research Communications

Neuroscience Research Communications

Volume 35, Issue 2, pages 83–95, September/October 2004

Additional Information

How to Cite

Armstrong, B. D., Paik, E., Chhith, S., Lelievre, V., Waschek, J. A. and Howard, S. G. (2004), Potentiation of (DL)-3,4-methylenedioxymethamphetamine (MDMA)-induced toxicity by the serotonin 2A receptior partial agonist d-lysergic acid diethylamide (LSD), and the protection of same by the serotonin 2A/2C receptor antagonist MDL 11,939. Neurosci. Res. Comm., 35: 83–95. doi: 10.1002/nrc.20023

Author Information

  1. 1

    Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, California

  2. 2

    Department of Pharmacology, University of California, Los Angeles, California

*Dept. of Psychiatry and Biobehavioral Sciences, University of California, 760 Westwood Plaza, N.P.I. 67-373, Los Angeles, California 90024

Publication History

  1. Issue published online: 26 OCT 2004
  2. Article first published online: 26 OCT 2004
  3. Manuscript Accepted: 23 JUL 2004

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Keywords:

  • MDMA;
  • ecstasy;
  • neurotoxicity;
  • LSD;
  • dopamine;
  • serotonin

Abstract

To elucidate the role of the serotonin (5-HT)2A/2C receptors in 3,4-methylenedioxymethamphetamine (MDMA)-induced neurotoxicity, MDMA was administered to rats and the presence of the serotonin transporter (5-HTT) was assessed at the protein level with immunohistochemistry (IHC), and the RNA level with a Northern blotting technique. d-lysergic acid diethylamide (LSD) and MDL 11,939 were given in conjunction with MDMA in order to assess the importance of 5-HT receptors in MDMA-induced neurotoxicity. The hypothesis is that the MDMA + LSD-treated animals should have more neurotoxicity as measured by loss of 5-HTTs compared to the MDMA-treated animals. Moreover, the loss of 5-HTTs should be attenuated in animals given the combination of MDMA + MDL 11,939, as the latter drug is a selective 5-HT2A/2C antagonist. The results showed that MDMA-induced neurotoxicity was dose dependently increased by LSD. Moreover, the drug MDL 11,939 attenuated MDMA-induced neurotoxicity, suggesting that 5-HT2A/2C receptors are involved in MDMA-induced neurotoxicity.

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