Acute and Chronic 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine Administrations Elicit Similar Microglial Activation in the Substantia Nigra of Monkeys

Increasing evidence suggests a pivotal role for neuroinflammation in the pathogenesis of Parkinson disease, but whether activated microglia participate in disease progression remains unclear. To clarify this issue, we determined the numbers of activated microglial cells in the substantia nigra pars...

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Veröffentlicht in:Journal of neuropathology and experimental neurology 2009-09, Vol.68 (9), p.977-984
Hauptverfasser: Vázquez-Claverie, Marianne, Garrido-Gil, Pablo, San Sebastián, Waldy, Izal-Azcárate, Amaya, Belzunegui, Silvia, Marcilla, Irene, López, Berta, Luquin, María-Rosario
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container_issue 9
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container_title Journal of neuropathology and experimental neurology
container_volume 68
creator Vázquez-Claverie, Marianne
Garrido-Gil, Pablo
San Sebastián, Waldy
Izal-Azcárate, Amaya
Belzunegui, Silvia
Marcilla, Irene
López, Berta
Luquin, María-Rosario
description Increasing evidence suggests a pivotal role for neuroinflammation in the pathogenesis of Parkinson disease, but whether activated microglia participate in disease progression remains unclear. To clarify this issue, we determined the numbers of activated microglial cells in the substantia nigra pars compacta and ventral tegmental area of monkeys subacutely and chronically exposed to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Monkeys in the subacute MPTP treatment group were killed 1 week after the last MPTP injection; chronically treated monkeys were killed either 6 or 35 months after the last MPTP injection. Subacute MPTP administration induced loss of dopaminergic neurons in the substantia nigra pars compacta and ventral tegmental area and microglial activation in the same areas. Chronic MPTP treatment resulted in greater dopaminergic neuron depletion in both treatment groups. Both groups of chronic MPTP-treated monkeys showed increased numbers of activated microglial cells in the substantia nigra pars compacta that were similar to those of the subacute MPTP treatment group. These results indicate that microglial activation seems to be induced mainly by the toxic effects of MPTP and that it does not further progress once the toxin administration has been terminated. This suggests that the progressive degeneration of nigral cells in Parkinson disease may not necessarily be associated with progressively increased microglial activation.
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These results indicate that microglial activation seems to be induced mainly by the toxic effects of MPTP and that it does not further progress once the toxin administration has been terminated. This suggests that the progressive degeneration of nigral cells in Parkinson disease may not necessarily be associated with progressively increased microglial activation.</abstract><cop>Hagerstown, MD</cop><pub>American Association of Neuropathologists, Inc</pub><pmid>19680145</pmid><doi>10.1097/NEN.0b013e3181b35e41</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record>
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subjects 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine - administration & dosage
Animals
Biological and medical sciences
Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases
Immunohistochemistry
Inflammation - chemically induced
Inflammation - immunology
Macaca fascicularis
Male
Medical sciences
Microglia - drug effects
Microglia - metabolism
Microglia - pathology
MPTP Poisoning - immunology
MPTP Poisoning - metabolism
MPTP Poisoning - pathology
Nerve Degeneration - metabolism
Nerve Degeneration - pathology
Neurology
Neurons - drug effects
Neurons - pathology
Neurotoxins - administration & dosage
Substantia Nigra - drug effects
Substantia Nigra - immunology
Substantia Nigra - metabolism
title Acute and Chronic 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine Administrations Elicit Similar Microglial Activation in the Substantia Nigra of Monkeys
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