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Gender difference in Parkinson’s disease (PD) suggests that female sex steroids may promote dopaminergic neuron survival and protect them from degeneration. The glial cell line-derived neurotrophic factor (GDNF) is believed to be dopaminotrophic; thus it is considered as a potential therapeutic target in PD. Additionally, GDNF is endogenously synthetized in the caudate/putamen of humans and striatum in rodents. A neuroprotective role of estrogens on the nigrostriatal pathway via the stimulation of GDNF has been proposed. Since the GDNF-producing parvalbumin (Parv) interneurons express the estrogen receptor alpha in the mouse striatum, we sought to determine whether ectopic estrogenic compound modulates the GDNF synthesis in mice. Using an ovariectomized-estradiol (E 2 ) replacement regimen, which reliably generates a rise of plasma estradiol, we assessed the effects of different levels of E 2  on the activation of striatal neuronal populations, and GDNF production. A strong correlation was found between plasma E 2  and the expression of the immediate early gene cFos in the striatum, as well as in other cortical regions. However, moderate and high E 2  treatments failed to induce any striatal GDNF mRNA and protein synthesis. High E 2  only stimulates cFos induction in a low percentage of striatal Parv neurons whereas the majority of cFos-positive cells are medium spiny neurons. Activation of these projecting neurons by E 2  suggests a role of circulating sex steroids in the modulation of striatal neural pathways.

Striatal GDNF Production Is Independent to Circulating Estradiol Level Despite Pan-Neuronal Activation in the Female Mouse