Early loss of dopaminergic terminals in striosomes after MDMA administration to mice
Noelia Granado, Isabel Escobedo, Esther O’shea, María Isabel Colado, Rosario Moratalla
Synapse October 25, 2007 DOI: 10.1002/syn.20466 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Experimental study Peer reviewed |
|---|---|
| Population | Mice |
| Intervention | MDMA |
| Topics | MDMA |
| Keywords | Striatum Dopaminergic Amphetamine Dopamine transporter Pharmacology Neurotoxicity |
| Citations | 59 |
| Key findings | MDMA caused significantly greater reductions in tyrosine hydroxylase and dopamine transporter immunostaining in striosomes than in the matrix compartment of the mouse striatum, indicating differential vulnerability of these compartments to MDMA-induced neurotoxicity. |
Abstract
Abstract The amphetamine analogue 3,4‐methylenedioxymethamphetamine (MDMA or “Ecstasy”) is a popular drug of abuse which causes different neurotoxic effects in the mouse compared with the rat. In mice, MDMA produces damage to striatal dopamine terminals, having little long‐term effects on serotonin (5‐HT) containing neurons. A relevant feature of the striatum is its striosome/matrix compartmental organization; defined by different connexions, and functions. In this study we examined the long‐term effect induced by MDMA on tyrosine hydroxylase (TH) and dopamine transporter (DAT) immunoreactivity in the striosomes and matrix compartments of mouse striatum. Mice given MDMA showed significant reductions in TH and DAT immunostaining in striatum compared with control animals. Interestingly, this effect was considerably more pronounced in striosomes than in the matrix. These data provide the first evidence that striosomes and matrix compartments of the mouse striatum have differential vulnerability to MDMA and that the long‐term neurotoxicity induced by MDMA in mice is primarily associated with a loss of striosomal dopamine fibres. Synapse 62:80–84, 2008. © 2007 Wiley‐Liss, Inc.
Comparable studies
Other preclinical and animal studies on MDMA, most cited first.
Citations in the library
Cited by 15
- Dopamine D2-receptor knockout mice are protected against dopaminergic neurotoxicity induced by methamphetamine or MDMA Neurobiology of Disease March 22, 2021
- Persistent MDMA‐induced dopaminergic neurotoxicity in the striatum and substantia nigra of mice Journal of Neurochemistry September 24, 2008
- Pharmacokinetics and pharmacodynamics of 3,4-methylenedioxymethamphetamine (MDMA): interindividual differences due to polymorphisms and drug–drug interactions Critical Reviews in Toxicology October 3, 2012
- Separating the agony from ecstasy: R(−)-3,4-methylenedioxymethamphetamine has prosocial and therapeutic-like effects without signs of neurotoxicity in mice Neuropharmacology October 6, 2017
- Microglial and astroglial activation by 3,4‐methylenedioxymethamphetamine (MDMA) in mice depends on S(+) enantiomer and is associated with an increase in body temperature and motility Journal of Neurochemistry October 20, 2012
and 10 more in the library
Cites 2
- Superoxide radicals mediate the biochemical effects of methylenedioxymethamphetamine (MDMA): Evidence from using CuZn‐superoxide dismutase transgenic mice Synapse October 1, 1995
- The pharmacology and clinical pharmacology of 3,4-methylenedioxymethamphetamine (MDMA, "ecstasy"). Pharmacological Reviews September 2003