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Publication : Implication of GPER1 in neuroprotection in a mouse model of Parkinson's disease.

First Author  Bourque M Year  2013
Journal  Neurobiol Aging Volume  34
Issue  3 Pages  887-901
PubMed ID  22749492 Mgi Jnum  J:194435
Mgi Id  MGI:5473764 Doi  10.1016/j.neurobiolaging.2012.05.022
Citation  Bourque M, et al. (2013) Implication of GPER1 in neuroprotection in a mouse model of Parkinson's disease. Neurobiol Aging 34(3):887-901
abstractText  This study investigated the contribution of the new G protein-coupled estrogen receptor 1 (GPER1) in neuroprotection by 17beta-estradiol in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson's disease. In intact mice, administration of GPER1 agonist G1 reproduced the effect of 17beta-estradiol in increasing striatal dopamine metabolite concentrations as well as the turnover of dopamine. GPER1 antagonist G15 blocked the effect of G1 on homovanillic acid/dopamine ratio and partially for 17beta-estradiol. MPTP mice treated with G15 were more susceptible to MPTP toxicity with a greater decrease in striatal dopamine concentration and dopamine transporter specific binding. In MPTP mice, dopamine concentrations as well as dopamine and vesicular monoamine transporter 2 specific binding showed that G1 treatment was as potent as 17beta-estradiol in protecting striatum and substantia nigra. G15 antagonized completely the neuroprotective effects of G1 in the striatum and substantia nigra as well as protection by 17beta-estradiol in the striatum but partially in the substantia nigra. This study showed an important role of GPER1 in neuroprotection and that G1 is as potent as 17beta-estradiol in mediating beneficial effects.
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