Chronic exposure to stress hormones alters the subtype of store‐operated channels expressed in H19‐7 hippocampal neuronal cells. Issue 6 (25th February 2013)

• Record Type: Journal Article
• Authors: Piron, Matthew; Villereal, Mitchel L.
• Is Part Of: Journal of cellular physiology. Volume 228:Issue 6(2013:Jun.)
• Page Start: 1332
• Page End: 1343
• Publication Date: 2013-02-25
• Subjects: Physiology -- Periodicals; Cell physiology -- Periodicals; 571.6
• DOI: 10.1002/jcp.24289
• Languages: English
• ISSNs: 0021-9541

Abstract

<abstract abstract-type="main" xml:lang="en"> <title>Abstract</title> <p>Differentiating H19‐7 hippocampal precursor cells up‐regulate (∼4.3‐fold) store‐operated channel (SOC) activity; relatively linear current‐voltage curves indicate an I<sub>SOC</sub> subtype of SOC. In differentiated H19‐7 neurons, the majority of agonist (arginine vasopressin, AVP)‐stimulated Ca<sup>2+</sup> 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<sup>2+</sup> entry (SOCE) and inhibition of AVP‐stimulated Ca<sup>2+</sup> entry. Treatment of H19‐7 cells with the rat stress hormone corticosterone during differentiation induces a significant increase in AVP‐stimulated Ca<sup>2+</sup> entry, which is virtually eliminated by 2‐APB, suggesting a corticosterone‐induced increase of SOCE. Corticosterone also enhances AVP‐stimulated Mn<sup>2+</sup> entry, confirming an elevated Ca<sup>2+</sup> entry pathway, rather than a decreased Ca<sup>2+</sup> 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<sup>2+</sup> 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<sub>CRAC</sub> subtype of SOCs. Consistent with this finding is the observation that corticosterone treatment of H19‐7 cells increases the expression of the I<sub>CRAC</sub> channel subunit Orai1. Thus, the subtype of SOCs expressed in H19‐7 hippocampal neurons can be altered from I<sub>SOC</sub> to I<sub>CRAC</sub> by chronic treatment with stress hormones. J. Cell. Physiol. 228: 1332–1343, 2013. © 2012 Wiley Periodicals, Inc.</p> </abstract>