Cytoplasmic aggregates of phosphorylated extracellular signal-regulated protein kinases in Lewy body diseases.
The mechanism of estrogen-mediated neuroprotection is not yet clear. Estrogens have a variety of modes of action including transducing signaling events such as activation and/or suppression of the MAPK pathway. We have previously shown protein phosphatases to be involved in 17β-estradiol mediated neuroprotection. In the present study, we assessed the role of estrogen-receptors (ER) in estrogen-mediated neuroprotection from oxidative/excitotoxic stress and the consequential effects on MAPK signaling. Okadaic acid and calyculin A, non-specific serine/threonine phosphatase inhibitors, were exposed to cells at various concentrations in the presence or absence of 17α-estradiol, the enantiomer of 17β-estradiol,