Electrophysiological responses to bradykinin and microinjected inositol polyphosphates in neuroblastoma cells
FEBS LettersPublished 20 April 1987Open access
Leon G.J. Tertoolen, Ben C. Tilly, Robin F. Irvine, Wouter H. Moolenaar
Citations46
SJR quartileQ1
SJR score1.22
SNIP0.77
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TL;DR
It is suggested that, while IP3(1,4,5) triggers the release of stored Ca2+ to hyperpolarize the membrane, IP3 (1,3,4) may initiate a membrane depolarization.
Abstract
Addition of bradykinin to mouse N1E-115 neuroblastoma cells evokes a rapid but transient rise in cytoplasmic free Ca2+ concentration ([Ca2+]i). The [Ca2+]i rise is accompanied by a transient membrane hyperpolarization, due to a several-fold increase in K+ conductance, followed by a prolonged depolarizing phase. Pretreatment of the cells with a Ca2+-ionophore abolishes the hormone-induced hyperpolarization but leaves the depolarizing phase intact. The transient hyperpolarization can be mimicked by iontophoretic injection of IP3(1,4,5) or Ca2+, but not by injection of IP3(1,3,4), IP4(1,3,4,5) or Mg2+ into the cells. Instead, IP3(1,3,4) evokes a small but significant membrane depolarization in about 50% of the cells tested. Microinjected IP4(1,3,4,5) has no detectable effect, nor has treatment of the cells with phorbol esters. These results suggest that, while IP3(1,4,5) triggers the release of stored Ca2+ to hyperpolarize the membrane, IP3(1,3,4) may initiate a membrane depolarization.
Keywords
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