Vulnerability to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) toxicity in adolescent mice chronically treated with 3,4-methylenedioxymethamphetamine (MDMA) (Abstract/Poster in atti di convegno)

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Label
  • Vulnerability to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) toxicity in adolescent mice chronically treated with 3,4-methylenedioxymethamphetamine (MDMA) (Abstract/Poster in atti di convegno) (literal)
Anno
  • 2012-01-01T00:00:00+01:00 (literal)
Alternative label
  • Costa G. (1), Pinna A. (1,2), Frau L. (1) & Morelli M. (1,2,3) (2012)
    Vulnerability to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) toxicity in adolescent mice chronically treated with 3,4-methylenedioxymethamphetamine (MDMA)
    in 8th FENS Forum of Neuroscience, Barcellona, Spagna, 14-18 Luglio
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Costa G. (1), Pinna A. (1,2), Frau L. (1) & Morelli M. (1,2,3) (literal)
Note
  • Poster (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • (1) Department of Biomedical Sciences, University of Cagliari, Cagliari, Italy; (2) CNR Institute of Neuroscience, Cagliari, Italy; (3) Centre of Excellence for Neurobiology of Dependence, Cagliari, Italy (literal)
Titolo
  • Vulnerability to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) toxicity in adolescent mice chronically treated with 3,4-methylenedioxymethamphetamine (MDMA) (literal)
Abstract
  • Parkinson's disease (PD) is caused by a loss of dopamine-containing neurons in the substantia nigra pars compacta (SNc). Although the origin of this degeneration is unknown, environmental factors and amphetamine-like drugs of abuse, as well as neuroinflammation, might contribute to PD-associated neuronal loss. Since several reports suggest that 3,4 methylenedioxymethamphetamine (MDMA, 'Ecstasy') induces neurotoxic and neuroinflammatory effects in experimental animals, we evaluated if the adolescent brain, which may be highly susceptible to drug-induced neurotoxicity, shows higher vulnerability to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) after a subchronic exposure to MDMA. To this end the study examined the activation of glial cells and the vulnerability of dopaminergic neurons to the administration of MPTP in C57BL/6J mice treated from the adolescence to the adult age with MDMA. Mice received MDMA (10 mg/kg i.p.) or vehicle according to a 9-weeks administration schedule. MDMA strongly increased CD11b immunoreactivity at 4 days after MDMA administration, while, at 7 days, CD11b immunoreactivity was similar to the saline control. GFAP immunoreactivity peaked at 4 days and persisted at 7 days. Mice which received MPTP (20 mg/kg i.p.) or vehicle two weeks after the last MDMA or vehicle administration, showed a loss of TH-positive neurons, and an increases the expression of GFAP and CD11b in both striatum and SNc compared with vehicle. Previous administration of MDMA amplified the GFAP and CD11b immunoreactivity and the loss of TH-positive neurons in both SNc and striatum. In conclusion, our results suggest that MDMA administered during adolescence in mice exacerbates the neurodegeneration and neuroinflammation caused by MPTP. (literal)
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