INIMEC - CONICET   05467
INSTITUTO DE INVESTIGACION MEDICA MERCEDES Y MARTIN FERREYRA
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Activation of ERK1/2 and axogenesis induced by estradiol depend on different calcium pools in male rat hypothalamic neurons in vitro
Autor/es:
BOLLO, M.; CAMBIASSO, M.J.; CABRERA ZAPATA, L.E.
Lugar:
CABA
Reunión:
Congreso; 2do. Congreso de la Federación de Sociedades de Neurociencias de Latinoamérica y el Caribe (FALAN); 2016
Institución organizadora:
Sociedad Argentina de Investigación en Neurociencias
Resumen:
Estradiol (E2)induces axonal growth through the extracellular signal-regulated kinase 1 and 2(ERK1/2) cascade in hypothalamic neurons of male rat embryos in vitro. Both axogenesis and ERK1/2 activationmediated by E2 depend on Ca2+ and Ca2+-dependent PKC isoforms.In the present study we investigated the Ca2+ pools that participatein the activation of ERK1/2 and axogenesis by E2. Hypothalamic neuron cultureswere established from male rat embryos of 16 days of gestation and fed withastroglia-conditioned media for 48 hours. E2 treatment rapidly induced ERK phosphorylation,which was completely abolished by a ryanodine receptor (RyR) inhibitor(ryanodine) and partially attenuated by an L-type voltage-gated Ca2+channel (L-VGCC) blocker (nifedipine) and aninositol-1,4,5-trisphosphate receptor (IP3R) inhibitor (2-APB). EGTAslightly decreased E2-induced ERK1/2 phosphorylation but this effect was notstatistically significant. In regard to E2-induced axonal growth, it was completelyinhibited by ryanodine. Furthermore, we are currently conducting Ca2+imaging recording using primary cultured neurons that over-express agenetically-encoded Ca2+-indicator (GCaMP6s). Preliminary results suggestthat E2 induces Ca2+oscillations, which, at least in part, depend onCa2+influx. In summary, the results suggest that Ca2+mobilization from extracellular space as well as from endoplasmic reticulum arenecessary to E2-induced ERK1/2 activation and axogenesis. Besides, whereasL-VGCCs and IP3Rs might participate in the Ca2+ signalingevoked by E2, the predominant role is mediated by RyRs.Financial support: CONICET, ANPCyT andSECyT-UNC, Argentina.