Sex differences in cell genesis, hippocampal volume and behavioral outcomes in a rat model of neonatal HI.

摘要: Hypoxia-ischemia (HI) of the brain in near-term and term infants is a leading cause infant mortality lifelong disability but current therapeutic approaches remain limited. Males consistently display greater vulnerability to deleterious consequences HI both humans animal models. Neurogenesis increases after neonatal offers potential target for recovery. The steroid hormone estradiol has been extensively explored as neuroprotectant adult models stroke with mixed results. Less consideration afforded this naturally occurring agent developing brain, which unique challenges from adult. Using model rat we have impact insult on cell genesis hippocampus males females ability treatment immediately restore function. Both short-term (3 days) long-term (7 post-injury were assessed revealed that only had markedly increased sexes long-term. A battery behavioral tests motor impairment compromised episodic memory while modestly impaired spatial memory. Juvenile social play was also depressed HI. Estradiol therapy improved performance did not reverse deficit hippocampal volume ipsilateral insult. Thus effects do appear be via death or proliferation rather involve other components neural functioning.