Movement Disorders
September 20, 2013
Giulia Costa, Lucia Frau, Jadwiga Wardas et al.
52 citations
Chronic administration of MDMA (ecstasy) during late adolescence in mice worsens the brain damage caused by MPTP, a toxin that induces Parkinson's disease (PD) in humans. Mice treated twice daily with MDMA (10 mg/kg) from 8 to 17 weeks of age, then given MPTP (20 mg/kg four times), showed greater activation of microglia and astroglia in the striatum and substantia nigra pars compacta (SNc) compared to mice given only MPTP or vehicle. This neuroinflammation was accompanied by a greater loss of dopamine-producing neurons (indicated by reduced tyrosine hydroxylase immunoreactivity) in the SNc and striatum. The findings suggest that MDMA use may increase the risk of dopaminergic neuron degeneration.
Journal of Neurochemistry
October 20, 2012
Lucia Frau, Nicola Simola, Antonio Plumitallo et al.
46 citations
The S(+) enantiomer of MDMA, but not the R(−) enantiomer, activates microglia and astroglia in the mouse striatum, though less strongly than racemic MDMA. Combining both enantiomers produces no greater activation than S(+) alone. Only racemic MDMA slightly activates microglia in other brain regions. S(+) and racemic MDMA similarly increase motor activity and body temperature, while R(−) has no effect. Body temperature rise correlates with glial activation. The findings indicate additive rather than synergistic effects of the two enantiomers and highlight the need to study their separate contributions to MDMA's neuroinflammatory and neurotoxic effects.
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
May 1, 2023
Giulia Costa, Marcello Serra, Riccardo Maccioni et al.
13 citations
A standardized extract of Withania somnifera (ashwagandha), when given acutely alongside MDMA (ecstasy), protects mice from the drug's harmful effects on the brain, body temperature, and memory. MDMA alone caused degeneration of dopamine-producing neurons, inflammation (gliosis), a rise in body temperature, and impaired performance on a novel object recognition task. These effects were not prevented by pretreating mice with the extract for three days before MDMA. However, when the extract was given together with MDMA, it counteracted the loss of dopamine neurons in the substantia nigra, reduced gliosis in the striatum, normalized body temperature, and restored memory performance to levels similar to those of saline-treated controls.