Elsevier

Neuroscience Letters

Volume 104, Issues 1–2, 25 September 1989, Pages 178-182
Neuroscience Letters

Reserpine does not prevent 3,4-methylenedioxymethamphetamine-induced neurotoxicity in the rat

https://doi.org/10.1016/0304-3940(89)90351-0Get rights and content

Abstract

3,4-Methylenedioxymethamphetamine (MDMA; ‘Ecstasy’) is a known neurotoxin to 5-hydroxytryptamine (5-HT) nerve terminals. Recent studies have suggested that endogenous dopamine (DA) and/or 5-HT may mediate the MDMA-induced neurotoxicity. The central monoamine stores of rats were significantly decreased with reserpine (5 mg/kg) prior to toxic injections of MDMA. Rats given MDMA (30 mg/kg) displayed significant decreases in the density of 5-HT nerve terminals labeled by [3H]paroxetine both with (51 ± 8 %) and without (43 ± 20 %) reserpine pre-treatment. These data suggest that the degeneration of 5-HT nerve terminals following MDMA is independent of the presence of endogenous stores of DA or 5-HT.

References (16)

There are more references available in the full text version of this article.

Cited by (11)

  • Breathing new life into neurotoxic-based monkey models of Parkinson's disease to study the complex biological interplay between serotonin and dopamine

    2021, Progress in Brain Research
    Citation Excerpt :

    Previous data obtained in rats have suggested that the effects of MDMA, in particular the decrease in 5-HT concentration and the decrease in activity of tryptophan hydroxylase 2 (TPH2, the 5-HT synthetic enzyme), are based on an intact DA system (Brodkin et al., 1993; Schmidt et al., 1990; Stone et al., 1988). On the contrary, another study showed a persistent reduction of SERT fibers despite prior DA lesion (Hekmatpanah et al., 1989). If dopamine predisposes neurochemical and/or neurotoxic effects of MDMA, then the striatum should show a decrease in the binding of DASB in addicts to ecstasy, which is not the case (Kish et al., 2010).

View all citing articles on Scopus
View full text