Record Display for the EPA National Library Catalog


Main Title Characterization of the Origins of Astrocyte Response to Injury Using the Dopaminergic Neurotoxicant, 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydrophyridine.
Author O'Callaghan, J. P. ; Miller, D. B. ; Reinhard., J. F. ;
CORP Author Health Effects Research Lab., Research Triangle Park, NC. ;Wellcome Research Labs., Research Triangle Park, NC.
Publisher c25 Jun 90
Year Published 1990
Report Number EPA/600/J-90/231;
Stock Number PB91-117077
Additional Subjects Toxicology ; Nervous system ; Nerve cells ; Mice ; Reprints ; Astrocytes ; Methyl tetrahydropyridines ; Dopamine receptors ; Glial fibrillary acidic protein ; Radioimmunoassay ; Tyrosine hydroxylase ; Phosphoproteins ; Mitogens ; Interleukin-1
Library Call Number Additional Info Location Last
NTIS  PB91-117077 Some EPA libraries have a fiche copy filed under the call number shown. 07/26/2022
Collation 10p
The amount of glial fibrillary acidic protein (GFAP), an astrocyte protein, increases following injury of the CNS. A radioimmunoassay of GFAP was used to characterize the astrocytic response to injury resulting from exposure to the dopaminergic neurotoxicant, 1-methyl-1,2,3,6-tetrahydropyridine (MPTP). A single administration of MPTP to the C57BL/6 mouse resulted in more than a 3-fold increase in GFAP within 48 hours, followed by a decline to baseline at 3 weeks. A decrease in the amount of tyrosine hydroxylase (TH), a marker of nigrostriatal dopaminergic neurons, preceded the rise in GFAP. The concentration of DARPP-32, a phosphoprotein localized to striatal neurons receiving dopaminergic input, was not affected by MPTP. Protecting the dopaminergic neurons from the neurotoxic metabolite of MPTP, 1-methyl-4-phenylpyridinium (MPP+), either by blocking its formation or by preventing its uptake into dopamine neurons, completely blocked the increase in GFAP. Blood-borne or brain-derived interleukin 1 (IL-1), a known astrocyte mitogen, did not appear to mediate the effects of MPTP on GFAP. (Copyright (c) 1990 Elsevier Science Publishers B.V. (Biomedical Division))