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 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.
D000818:Animals; D001920:Bradykinin / Q000494:pharmacology*; D002118:Calcium / Q000378:metabolism / Q000494:pharmacology; D002460:Cell Line; D004594:Electrophysiology; D004987:Ethers / Q000494:pharmacology; D015544:Inositol 1,4,5-Trisphosphate; D007295:Inositol Phosphates / Q000494:pharmacology*; D015759:Ionomycin; D008564:Membrane Potentials / Q000187:drug effects; D008845:Microinjections; D009447:Neuroblastoma / Q000503:physiopathology*; D013403:Sugar Phosphates / Q000494:pharmacology*
D004987:Ethers; D007295:Inositol Phosphates; D013403:Sugar Phosphates; C081655:inositol-1,3,4,5-tetrakisphosphate; D015759:Ionomycin; D015544:Inositol 1,4,5-Trisphosphate; D001920:Bradykinin; D002118:Calcium