Because critical enzymes required for E2 synthesis, such as aromatase and StAR, are synaptically localized in hippocampal neurons and glial cells [51], the possibility arises that long-term OVX rats may retain the ability to produce some brain-derived E2 even after loss of circulating E2, and that E2 administered after ischemia may interact with locally synthesized E2 to protect neurons. The gene discussed is STAR; the disease is ischemia.