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Electrophysiological responses to bradykinin and microinjected inositol polyphosphates in neuroblastoma cells: Possible role of inositol 1,3,4-trisphosphate in altering membrane potential

Addition of bradykinin to mouse N1E-115 neuroblastoma cells evokes a rapid but transient rise in cytoplasmic free Ca 2+ concentration ([Ca 2+]i). The [Ca 2+] i rise is accompanied by a transient membrane hyperpolarization, due to a several-fold increase in K + conductance, followed by a prolonged de...

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Bibliographic Details
Published in:FEBS letters 1987-04, Vol.214 (2), p.365-369
Main Authors: Tertoolen, Leon G.J., Tilly, Ben C., Irvine, Robin F., Moolenaar, Wouter H.
Format: Article
Language:English
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Summary:Addition of bradykinin to mouse N1E-115 neuroblastoma cells evokes a rapid but transient rise in cytoplasmic free Ca 2+ concentration ([Ca 2+]i). The [Ca 2+] i rise is accompanied by a transient membrane hyperpolarization, due to a several-fold increase in K + conductance, followed by a prolonged depolarizing phase. Pre-treatment of the cells with a Ca 2+-ionophore abolishes the hormone-induced hyperpolarization but leaves the depolarizing phase intact. The transient hyperpolarization can be mimicked by iontophoretic injection of IP 3(1,4,5) or Ca 2+, but not by injection of IP 3(1,3,4), IP 4(1,3,4,5) or Mg 2+ into the cells. Instead, IP 3(1,3,4) evokes a small but significant membrane depolarization in about 50% of the cells tested. Microinjected IP 4(1,3,4,5) has no detectable effect, nor has treatment of the cells with phorbol esters. These results suggest that, while IP 3(1,4,5) triggers the release of stored Ca 2+ to hyperpolarize the membrane, IP 3(1,3,4) may initiate a membrane depolarization.
ISSN:0014-5793
1873-3468
DOI:10.1016/0014-5793(87)80089-3