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Estrogen Alters MPTP‐Induced Neurotoxicity in Female Mice: Effects on Striatal Dopamine Concentrations and Release
Author(s) -
Dluzen Dean E.,
McDermott Janet L.,
Liu Binjun
Publication year - 1996
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1996.66020658.x
Subject(s) - mptp , dopamine , estrogen , dopaminergic , endocrinology , medicine , neurotoxicity , chemistry , nigrostriatal pathway , ovariectomized rat , biology , toxicity , substantia nigra
The effects of estrogen on MPTP‐induced neurotoxicity of the nigrostriatal dopaminergic system were examined in C57Bl and CD‐1 mice. Ovariectomized mice with and without estrogen were treated with MPTP or its vehicle. The effects of these treatments on striatal dopamine concentrations and l ‐DOPA‐stimulated dopamine and l ‐3,4‐dihydroxyphenylacetic acid (DOPAC) release in vitro were determined. Dopamine concentrations of C57Bl mice receiving estrogen before MPTP were significantly greater than those of non‐estrogen‐treated MPTP mice as well as estrogen‐treated mice receiving the MPTP vehicle. Dopamine concentrations of the CD‐1 mice did not differ with these treatments. l ‐DOPA‐evoked dopamine release values of estrogen‐treated C57Bl mice were significantly increased compared with non‐estrogen‐treated mice. No such differences were observed in the MPTP‐treated C57Bl mice. DOPAC release rates were similar to that of dopamine in these C57Bl mice. In the CD‐1 mice estrogen also produced a significant increase in l ‐DOPA‐evoked dopamine release; however, this response was unaltered by MPTP treatment. A significant increase in l ‐DOPA‐evoked DOPAC output was obtained only for estrogen‐treated CD‐1 mice. Both strains show very similar responses to the estrogen treatment, but differential responses of dopamine release to l ‐DOPA between the C57Bl and CD‐1 mice were obtained with regard to the interactive effects of estrogen and MPTP. Our results suggest that in addition to its role as modulator, estrogen may also function as a neuroprotectant against MPTP neurotoxicity of the nigrostriatal dopaminergic system in the C57Bl mouse.