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Electrophysiological responses to bradykinin and microinjected inositol polyphosphates in neuroblastoma cells
Author(s) -
Tertoolen Leon G.J.,
Tilly Ben C.,
Irvine Robin F.,
Moolenaar Wouter H.
Publication year - 1987
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(87)80089-3
Subject(s) - depolarization , hyperpolarization (physics) , bradykinin , biophysics , membrane potential , ionophore , inositol , electrophysiology , endocrinology , chemistry , medicine , biology , membrane , biochemistry , stereochemistry , receptor , nuclear magnetic resonance spectroscopy
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.