“…For instance, E2 dramatically reduces brain infarction volume after stroke (Groger & Plesnila, 2014), and through inhibiting NMDA receptors, it attenuates death of hippocampal neurons caused by quinolinic acid (Heron & Daya, 2001), NMDA (Park-Chung, Gibbs, & Farb, 1997), and glutamate (Hilton, Nunez, Bambrick, Thompson, & McCarthy, 2006). In addition to neuroprotection, E2 promotes recovery of neurological function from stroke (Groger & Plesnila, 2014), and reverses malfunction in synaptic plasticity by modulating NMDA receptors (Galvin & Ninan, 2014;Smith, Smith, Bredemann, & McMahon, 2016;Smith & McMahon, 2006;Snyder, Cooke, & Woolley, 2011). Therefore, we hypothesized that E2 might have therapeutic potential for TBI in both neuroprotection and recovery of neurological function.…”