Methylenedioxymethamphetamine-induced suppression of interleukin-1 beta and tumour necrosis factor-alpha is not mediated by serotonin

Research output: Contribution to a Journal (Peer & Non Peer)Articlepeer-review

Abstract

The purpose of the present study was to examine the role of serotonin release in methylenedioxymethamphetamine (MDMA)-induced immunosuppression in rats. We examined the effect of pretreatment with the selective serotonin reuptake inhibitor paroxetine, and the tryptophan hydroxylase inhibitor para-chlorophenylalanine on MDMA-induced suppression of interleukin-1 beta and tumour necrosis factor (TNF)-alpha secretion following an in vivo lipopolysaccharide challenge. Although paroxetine blocked MDMA-induced serotonin depletion in the cortex and hypothalamus, it failed to alter the suppressive effect of MDMA on lipopolysaccharide-induced TNF-alpha secretion. Similarly, although para-chlorophenylalanine caused a 90% depletion in cortical and hypothalamic serotonin content, it failed to alter the suppressive effect of MDMA on lipopolysaccharide-induced interleukin-1 beta or TNF-alpha secretion. In conclusion, although MDMA is a potent releaser of serotonin, the suppressive effects of MDMA on lipopolysaccharide-induced proinflammatory cytokine secretion cannot be attributed to its serotonin-releasing properties. (C) 2001 Elsevier Science B.V. All rights reserved.
Original languageEnglish (Ireland)
Number of pages5
JournalEuropean Journal Of Pharmacology
Volume418
Publication statusPublished - 1 Apr 2001

Authors (Note for portal: view the doc link for the full list of authors)

  • Authors
  • Connor, TJ;Dennedy, MC;Harkin, A;Kelly, JP

Fingerprint

Dive into the research topics of 'Methylenedioxymethamphetamine-induced suppression of interleukin-1 beta and tumour necrosis factor-alpha is not mediated by serotonin'. Together they form a unique fingerprint.

Cite this