MPTP-induced dopamine neuron degeneration and glia activation is potentiated in MDMA-pretreated mice.
Identifieur interne : 003D38 ( Ncbi/Merge ); précédent : 003D37; suivant : 003D39MPTP-induced dopamine neuron degeneration and glia activation is potentiated in MDMA-pretreated mice.
Auteurs : Giulia Costa [Italie] ; Lucia Frau ; Jadwiga Wardas ; Annalisa Pinna ; Antonio Plumitallo ; Micaela MorelliSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2013.
English descriptors
- KwdEn :
- Adrenergic Uptake Inhibitors (toxicity), Animals, Antigens, CD11b (metabolism), Brain (pathology), Cell Count, Disease Models, Animal, Dopaminergic Neurons (pathology), Drug Synergism, Glial Fibrillary Acidic Protein (metabolism), MPTP Poisoning (pathology), Male, Mice, Mice, Inbred C57BL, N-Methyl-3,4-methylenedioxyamphetamine (toxicity), Neuroglia (drug effects), Neuroglia (metabolism), Time Factors, Tyrosine 3-Monooxygenase (metabolism).
- MESH :
- chemical , metabolism : Antigens, CD11b, Glial Fibrillary Acidic Protein, Tyrosine 3-Monooxygenase.
- chemical , toxicity : Adrenergic Uptake Inhibitors, N-Methyl-3,4-methylenedioxyamphetamine.
- drug effects : Neuroglia.
- metabolism : Neuroglia.
- pathology : Brain, Dopaminergic Neurons, MPTP Poisoning.
- Animals, Cell Count, Disease Models, Animal, Drug Synergism, Male, Mice, Mice, Inbred C57BL, Time Factors.
Abstract
Clinical observations report a greater propensity to develop Parkinson's disease (PD) in amphetamine users. 3,4-Methylenedioxymethamphetamine (MDMA; "ecstasy") is an amphetamine-related drug that is largely consumed by adolescents and young adults, which may have neuroinflammatory and neurotoxic effects. Here, the objective was to evaluate in mice whether consumption of MDMA during adolescence might influence the neuroinflammatory and neurotoxic effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a toxin known to induce PD in humans. The activation of astroglia and microglia by glial fibrillary acidic protein (GFAP) and complement receptor type 3 (CD11b) immunohistochemistry and the degeneration of dopaminergic neurons by tyrosine hydroxylase (TH) immunohistochemistry were evaluated. MPTP (20 mg/kg × 4) was administered to mice treated from ages 8 weeks to 17 weeks with MDMA (10 mg/kg twice daily, two times a week). In mice that were chronically treated with MDMA, administration of MPTP induced a higher microglial and astroglial response in both the striatum and the substantia nigra pars compacta (SNc) compared with vehicle-treated or vehicle + MPTP-treated mice. Inflammatory changes were associated with a decrease in TH immunoreactivity in the SNc of MDMA-treated mice and with a further decrease in the striatum and the SNc of MDMA + MPTP-treated mice compared with vehicle-treated, MDMA-treated, and MPTP-treated mice. The results demonstrate that chronic administration of MDMA during late adolescence in mice exacerbates the neurodegeneration and neuroinflammation caused by MPTP, suggesting that MDMA may constitute a risk factor for dopaminergic neuron degeneration.
DOI: 10.1002/mds.25646
PubMed: 24108425
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pubmed:24108425Le document en format XML
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<author><name sortKey="Frau, Lucia" sort="Frau, Lucia" uniqKey="Frau L" first="Lucia" last="Frau">Lucia Frau</name>
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<author><name sortKey="Wardas, Jadwiga" sort="Wardas, Jadwiga" uniqKey="Wardas J" first="Jadwiga" last="Wardas">Jadwiga Wardas</name>
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<term>Brain (pathology)</term>
<term>Cell Count</term>
<term>Disease Models, Animal</term>
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<term>Drug Synergism</term>
<term>Glial Fibrillary Acidic Protein (metabolism)</term>
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<term>Male</term>
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<term>N-Methyl-3,4-methylenedioxyamphetamine (toxicity)</term>
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<term>Disease Models, Animal</term>
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<front><div type="abstract" xml:lang="en">Clinical observations report a greater propensity to develop Parkinson's disease (PD) in amphetamine users. 3,4-Methylenedioxymethamphetamine (MDMA; "ecstasy") is an amphetamine-related drug that is largely consumed by adolescents and young adults, which may have neuroinflammatory and neurotoxic effects. Here, the objective was to evaluate in mice whether consumption of MDMA during adolescence might influence the neuroinflammatory and neurotoxic effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a toxin known to induce PD in humans. The activation of astroglia and microglia by glial fibrillary acidic protein (GFAP) and complement receptor type 3 (CD11b) immunohistochemistry and the degeneration of dopaminergic neurons by tyrosine hydroxylase (TH) immunohistochemistry were evaluated. MPTP (20 mg/kg × 4) was administered to mice treated from ages 8 weeks to 17 weeks with MDMA (10 mg/kg twice daily, two times a week). In mice that were chronically treated with MDMA, administration of MPTP induced a higher microglial and astroglial response in both the striatum and the substantia nigra pars compacta (SNc) compared with vehicle-treated or vehicle + MPTP-treated mice. Inflammatory changes were associated with a decrease in TH immunoreactivity in the SNc of MDMA-treated mice and with a further decrease in the striatum and the SNc of MDMA + MPTP-treated mice compared with vehicle-treated, MDMA-treated, and MPTP-treated mice. The results demonstrate that chronic administration of MDMA during late adolescence in mice exacerbates the neurodegeneration and neuroinflammation caused by MPTP, suggesting that MDMA may constitute a risk factor for dopaminergic neuron degeneration.</div>
</front>
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<Abstract><AbstractText>Clinical observations report a greater propensity to develop Parkinson's disease (PD) in amphetamine users. 3,4-Methylenedioxymethamphetamine (MDMA; "ecstasy") is an amphetamine-related drug that is largely consumed by adolescents and young adults, which may have neuroinflammatory and neurotoxic effects. Here, the objective was to evaluate in mice whether consumption of MDMA during adolescence might influence the neuroinflammatory and neurotoxic effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a toxin known to induce PD in humans. The activation of astroglia and microglia by glial fibrillary acidic protein (GFAP) and complement receptor type 3 (CD11b) immunohistochemistry and the degeneration of dopaminergic neurons by tyrosine hydroxylase (TH) immunohistochemistry were evaluated. MPTP (20 mg/kg × 4) was administered to mice treated from ages 8 weeks to 17 weeks with MDMA (10 mg/kg twice daily, two times a week). In mice that were chronically treated with MDMA, administration of MPTP induced a higher microglial and astroglial response in both the striatum and the substantia nigra pars compacta (SNc) compared with vehicle-treated or vehicle + MPTP-treated mice. Inflammatory changes were associated with a decrease in TH immunoreactivity in the SNc of MDMA-treated mice and with a further decrease in the striatum and the SNc of MDMA + MPTP-treated mice compared with vehicle-treated, MDMA-treated, and MPTP-treated mice. The results demonstrate that chronic administration of MDMA during late adolescence in mice exacerbates the neurodegeneration and neuroinflammation caused by MPTP, suggesting that MDMA may constitute a risk factor for dopaminergic neuron degeneration.</AbstractText>
<CopyrightInformation>© 2013 Movement Disorder Society.</CopyrightInformation>
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<ForeName>Giulia</ForeName>
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