Stroke in Estrogen Receptor-α–Deficient Mice

摘要: Background and Purpose —Recent evidence suggests that endogenous estrogens or hormone replacement therapy can ameliorate brain damage from experimental stroke. Protective mechanisms involve enhanced cerebral vasodilation during ischemic stress as well direct preservation of neuronal viability. We hypothesized if the intracellular estrogen receptor subtype-α (ERα) is important to estrogen’s signaling in brain, then ERα-deficient (knockout) (ERαKO) female mice would sustain exaggerated infarction after middle artery occlusion. Methods —The histopathology cresyl violet–stained tissues was evaluated reversible occlusion (2 hours, followed by 22 hours reperfusion) ERαKO transgenic wild-type (WT) (C57BL/6J background strain). End-ischemic blood flow mapping obtained additional murine cohorts using [14C]iodoantipyrine autoradiography. Results —Total hemispheric tissue not altered ERα deficiency mice: 51.9±10.6 mm3 versus 60.5±5.0 WT. Striatal equivalent, 12.2±1.7 13.4±1.0 WT mice, but cortical paradoxically smaller relative (20.7±4.5 30.6±4.1 WT). Intraocclusion parietal cortex higher than likely accounting for reduced this anatomic area. There were no differences stroke outcomes region genotype male animals. Conclusions —Loss does enhance animal, suggesting inhibits injury do depend on activation subtype.