PMID- 24108425
OWN - NLM
STAT- MEDLINE
DCOM- 20140729
LR  - 20171116
IS  - 1531-8257 (Electronic)
IS  - 0885-3185 (Linking)
VI  - 28
IP  - 14
DP  - 2013 Dec
TI  - MPTP-induced dopamine neuron degeneration and glia activation is potentiated in 
      MDMA-pretreated mice.
PG  - 1957-65
LID - 10.1002/mds.25646 [doi]
AB  - 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 x 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.
CI  - (c) 2013 Movement Disorder Society.
FAU - Costa, Giulia
AU  - Costa G
AD  - Department of Biomedical Sciences, Section of Neuropsychopharmacology, University 
      of Cagliari, Cagliari, Italy.
FAU - Frau, Lucia
AU  - Frau L
FAU - Wardas, Jadwiga
AU  - Wardas J
FAU - Pinna, Annalisa
AU  - Pinna A
FAU - Plumitallo, Antonio
AU  - Plumitallo A
FAU - Morelli, Micaela
AU  - Morelli M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130920
PL  - United States
TA  - Mov Disord
JT  - Movement disorders : official journal of the Movement Disorder Society
JID - 8610688
RN  - 0 (Adrenergic Uptake Inhibitors)
RN  - 0 (CD11b Antigen)
RN  - 0 (Glial Fibrillary Acidic Protein)
RN  - EC 1.14.16.2 (Tyrosine 3-Monooxygenase)
RN  - KE1SEN21RM (N-Methyl-3,4-methylenedioxyamphetamine)
SB  - IM
MH  - Adrenergic Uptake Inhibitors/*toxicity
MH  - Animals
MH  - Brain/*pathology
MH  - CD11b Antigen/metabolism
MH  - Cell Count
MH  - Disease Models, Animal
MH  - Dopaminergic Neurons/*pathology
MH  - Drug Synergism
MH  - Glial Fibrillary Acidic Protein/metabolism
MH  - MPTP Poisoning/*pathology
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - N-Methyl-3,4-methylenedioxyamphetamine/*toxicity
MH  - Neuroglia/drug effects/*metabolism
MH  - Time Factors
MH  - Tyrosine 3-Monooxygenase/metabolism
OTO - NOTNLM
OT  - CD11b
OT  - Parkinson's disease
OT  - basal ganglia
OT  - glial fibrillary acidic protein
OT  - neuroinflammation
EDAT- 2013/10/11 06:00
MHDA- 2014/07/30 06:00
CRDT- 2013/10/11 06:00
PHST- 2013/05/16 00:00 [received]
PHST- 2013/07/08 00:00 [revised]
PHST- 2013/07/23 00:00 [accepted]
PHST- 2013/10/11 06:00 [entrez]
PHST- 2013/10/11 06:00 [pubmed]
PHST- 2014/07/30 06:00 [medline]
AID - 10.1002/mds.25646 [doi]
PST - ppublish
SO  - Mov Disord. 2013 Dec;28(14):1957-65. doi: 10.1002/mds.25646. Epub 2013 Sep 20.