title: Chronic exposure to stress hormones alters the subtype of store-operated channels expressed in H19-7 hippocampal neuronal cells.
abstract: Differentiating H19-7 hippocampal precursor cells up-regulate (∼4.3-fold) store-operated channel (SOC) activity; relatively linear current-voltage curves indicate an I(SOC) subtype of SOC. In differentiated H19-7 neurons, the majority of agonist (arginine vasopressin, AVP)-stimulated Ca(2+) entry occurs via SOCs, based on 2-aminoethyldiphenylborinate (2-APB) inhibition data and the observation that transient receptor potential C1 (TRPC1) channel knock down cells show a dramatic reduction of thapsigargin-stimulated store-operated Ca(2+) entry (SOCE) and inhibition of AVP-stimulated Ca(2+) entry. Treatment of H19-7 cells with the rat stress hormone corticosterone during differentiation induces a significant increase in AVP-stimulated Ca(2+) entry, which is virtually eliminated by 2-APB, suggesting a corticosterone-induced increase of SOCE. Corticosterone also enhances AVP-stimulated Mn(2+) entry, confirming an elevated Ca(2+) entry pathway, rather than a decreased Ca(2+) extrusion. When corticosterone addition is delayed until after H19-7 cells have fully differentiated, it still elevates SOCE. In corticosterone-treated H19-7 cells, the knock down of TRPC1 no longer blocks thapsigargin-stimulated Ca(2+) entry suggesting that the subtype of SOCs expressed in H19-7 cells is altered by corticosterone treatment. Electrophysiological studies demonstrate that store-operated currents in corticosterone-treated H19-7 cells exhibit a highly inward rectifying current-voltage curve consistent with an I(CRAC) subtype of SOCs. Consistent with this finding is the observation that corticosterone treatment of H19-7 cells increases the expression of the I(CRAC) channel subunit Orai1. Thus, the subtype of SOCs expressed in H19-7 hippocampal neurons can be altered from I(SOC) to I(CRAC) by chronic treatment with stress hormones.
authors.affiliation: Department of Neurobiology, Pharmacology and Physiology, University of Chicago, Chicago, IL 60637, USA.
authors.forename: Matthew
authors.initials: M
authors.lastname: Piron
authors.forename: Mitchel L
authors.initials: ML
authors.lastname: Villereal
mesh_terms: D000818:Animals; D001127:Arginine Vasopressin / Q000378:metabolism; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels / Q000187:drug effects / Q000378:metabolism*; D002454:Cell Differentiation; D002460:Cell Line; D003345:Corticosterone / Q000378:metabolism*; D006624:Hippocampus / Q000187:drug effects / Q000196:embryology / Q000378:metabolism*; D008564:Membrane Potentials; D049990:Membrane Transport Modulators / Q000494:pharmacology; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*; D000071740:ORAI1 Protein; D053499:Plasma Membrane Calcium-Transporting ATPases / Q000378:metabolism; D034622:RNA Interference; D051381:Rats; D013312:Stress, Physiological / Q000187:drug effects; D050052:TRPC Cation Channels / Q000187:drug effects / Q000235:genetics / Q000378:metabolism*; D013997:Time Factors; D014162:Transfection
chemical_list: D015220:Calcium Channels; D049990:Membrane Transport Modulators; D000071740:ORAI1 Protein; C532493:Orai1 protein, rat; D050052:TRPC Cation Channels; C104603:TRPC3 cation channel; C096351:transient receptor potential cation channel, subfamily C, member 1; D001127:Arginine Vasopressin; D053499:Plasma Membrane Calcium-Transporting ATPases; D002118:Calcium; D003345:Corticosterone