Reserpine does not prevent 3,4-methylenedioxymethamphetamine-induced neurotoxicity in the rat.
C R Hekmatpanah, D J McKenna, Stephen J. Peroutka
Neuroscience Letters September 25, 1989 DOI: 10.1016/0304-3940(89)90351-0 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Animal experiment Peer reviewed |
|---|---|
| Population | Rats |
| Interventions | MDMA Reserpine |
| Dose | MDMA 30 mg/kg; reserpine 5 mg/kg |
| Measures | [3H]paroxetine labeling of 5-HT nerve terminals |
| Topics | MDMA |
| Key findings | MDMA (30 mg/kg) reduced [3H]paroxetine-labeled serotonin nerve terminal density by 51 +/- 8% after reserpine pretreatment and by 43 +/- 20% without it. The authors suggest that MDMA-induced degeneration of serotonin nerve terminals is independent of endogenous dopamine or serotonin stores. |
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.
Comparable studies
Other preclinical and animal studies on MDMA, most cited first.
Citations in the library
Cited by 5
- In vivo evidence for free radical involvement in the degeneration of rat brain 5‐HT following administration of MDMA (‘ecstasy’) and p‐chloroamphetamine but not the degeneration following fenfluramine British Journal of Pharmacology July 1, 1997
- The hyperthermic and neurotoxic effects of ‘Ecstasy’ (MDMA) and 3,4 methylenedioxyamphetamine (MDA) in the Dark Agouti (DA) rat, a model of the CYP2D6 poor metabolizer phenotype British Journal of Pharmacology August 1, 1995
- Vesicular monoamine transporter 2 and the acute and long-term response to 3,4-(±)-methylenedioxymethamphetamine. Toxicological sciences : an official journal of the Society of Toxicology January 2015
- The pharmacology and clinical pharmacology of 3,4-methylenedioxymethamphetamine (MDMA, "ecstasy"). Pharmacological Reviews September 2003
- The spin trap reagent alpha-phenyl-N-tert-butyl nitrone prevents 'ecstasy'-induced neurodegeneration of 5-hydroxytryptamine neurones. European Journal of Pharmacology July 14, 1995
Cites 8
- Methylenedioxyamphetamine (MDA) and methylenedioxymethamphetamine (MDMA) cause selective ablation of serotonergic axon terminals in forebrain: immunocytochemical evidence for neurotoxicity Journal of Neuroscience August 1, 1988
- Neurotoxicity of the psychedelic amphetamine, methylenedioxymethamphetamine. Journal of Pharmacology and Experimental Therapeutics 1987
- 3,4-Methylenedioxymethamphetamine and 3,4-methylenedioxyamphetamine destroy serotonin terminals in rat brain: quantification of neurodegeneration by measurement of [3H]paroxetine-labeled serotonin uptake sites. Journal of Pharmacology and Experimental Therapeutics September 1, 1987
- (±3,4-Methylenedioxymethamphetamine Selectively Damages Central Serotonergic Neurons in Nonhuman Primates JAMA July 1, 1988
- Role of endogenous dopamine in the central serotonergic deficits induced by 3,4-methylenedioxymethamphetamine. Journal of Pharmacology and Experimental Therapeutics October 1, 1988
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