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Main Title 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine (MPTP)-Induced Astrogliosis Does Not Require Activation of Ornithine Decarboxylase.
Author O'Callaghan, J. P. ; Seidler, F. J. ;
CORP Author Health Effects Research Lab., Research Triangle Park, NC. Neurotoxicology Div. ;Duke Univ. Medical Center, Durham, NC. Dept. of Pharmacology.
Publisher c1992
Year Published 1992
Report Number EPA/600/J-94/389;
Stock Number PB95-126496
Additional Subjects Astrocytes ; Gliosis ; Ornithine decarboxylase ; Enzyme activation ; Glial fibrillary acidic protein ; Polyamines ; Biosynthesis ; Blood-brain barrier ; Corpus striatum ; Hippocampus ; Reprints ; Pyridine/1-methyl-4-phenyl-1-2-3-6-tetrahydro
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NTIS  PB95-126496 Some EPA libraries have a fiche copy filed under the call number shown. 07/26/2022
Collation 8p
Abstract
Mechanical injury to the brain results is enhanced immunostaining for glial fibrillary acidic protein (GFAP) that is markedly inhibited by diffuoromethylornithine (DFMO), an irreversible inhibitor of ornithine decarboxlase. In the current study, systemic exposure of mice to the dopaminergic neurotoxicant, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), also increased GFAP but, unlike mechanical injury, this increase was not prevented by DFMO pretreatment. These results indicate that de novo polyamine biosynthesis is not obligatory for the MPTP-induced increase in GFAP. MPTP administration, unlike mechanical injury, does not disrupt the blood-brain barrier; thus, a role for polyamine biosynthesis in the astrocyte response to injury may be restricted to insults involving a compromised blood-brain barrier.