Morphological changes induced by CRH in mouse hippocampal neuronal cells

BONFIGLIO J.J.; INDA, C.; SENIN, S.; MACCARRONE, G.; TURCK, C. W.; HOLSBOER, F.; ARZT, E.; SILBERSTEIN, S.

Buenos Aires

Simposio; Workshop Fronteras en Biociencia, organizado por el Ministerio de Ciencia, Tecnología e Innovación Productiva de la República Argentina y la Sociedad Max Planck; 2012

Ministerio de Ciencia, Tecnología e Innovación Productiva de la República Argentina y la Sociedad Max Planck

CRH is the key mediator of the neuroendocrine, autonomic and behavioral responses to stress. Essential to the stress response are hypothalamic paraventricular CRH-secreting neurons that drive both basal and stress-induced hypothalamic-pituitary-adrenal axis (HPA) activation. CRH and other CRH-related ligands exert its action through G-protein-coupled receptors (GPCRs). CRH is a high affinity ligand for its type 1 receptor (CRHR1) and binds poorly to the type 2 receptor (CRHR2) for which other ligands such as urocortin II and III have more affinity. Our lab demonstrated that CRH, acting through CRHR1, activates a MAPK signal transduction pathway downstream PKA in cultured pituitary corticotrophs and in vivo in specific areas of the mouse brain (hippocampal subfields and basolateral complex of the amygdala). We are exploring the signaling network that mediates MAPK activation by CRH in hippocampal cell lines using molecular and pharmacological tools combined with proteomics.