Ramírez Barrantes, R.Carvajal Zamorano K., K.Rodríguez, B.Córdova, C.Lozano, C.Simón, F.Díaz, P.Muñoz, P.Marchant, I.Latorre, R.Castillo, K.Olivero, P.2021-11-232021-11-232020-05Frontiers in PhysiologyOpen AccessVolume 1126 May 2020 Article number 4441664-042Xhttp://repositorio.unab.cl/xmlui/handle/ria/21038Indexación: Scopus17β-estradiol is a neuronal survival factor against oxidative stress that triggers its protective effect even in the absence of classical estrogen receptors. The polymodal transient receptor potential vanilloid subtype 1 (TRPV1) channel has been proposed as a steroid receptor implied in tissue protection against oxidative damage. We show here that TRPV1 is sufficient condition for 17β-estradiol to enhance metabolic performance in injured cells. Specifically, in TRPV1 expressing cells, the application of 17β-estradiol within the first 3 h avoided H2O2-dependent mitochondrial depolarization and the activation of caspase 3/7 protecting against the irreversible damage triggered by H2O2. Furthermore, 17β-estradiol potentiates TRPV1 single channel activity associated with an increased open probability. This effect was not observed after the application of 17α-estradiol. We explored the TRPV1-Estrogen relationship also in primary culture of hippocampal-derived neurons and observed that 17β-estradiol cell protection against H2O2-induced damage was independent of estrogen receptors pathway activation, membrane started and stereospecific. These results support the role of TRPV1 as a 17β-estradiol-activated ionotropic membrane receptor coupling with mitochondrial function and cell survival. © Copyright © 2020 Ramírez-Barrantes, Carvajal-Zamorano, Rodriguez, Cordova, Lozano, Simon, Díaz, Muñoz, Marchant, Latorre, Castillo and Olivero.en17β-estradiolTRPV1NeuroprotectionMembrane receptorCell deathArtículoAtribución 4.0 Internacional (CC BY 4.0)10.3389/fphys.2020.00444