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.
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Authors | L G Tertoolen, B C Tilly, R F Irvine, W H Moolenaar |
Journal | FEBS letters
(FEBS Lett)
Vol. 214
Issue 2
Pg. 365-9
(Apr 20 1987)
ISSN: 0014-5793 [Print] England |
PMID | 3494634
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Ethers
- Inositol Phosphates
- Sugar Phosphates
- inositol-1,3,4,5-tetrakisphosphate
- Ionomycin
- Inositol 1,4,5-Trisphosphate
- Bradykinin
- Calcium
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Topics |
- Animals
- Bradykinin
(pharmacology)
- Calcium
(metabolism, pharmacology)
- Cell Line
- Electrophysiology
- Ethers
(pharmacology)
- Inositol 1,4,5-Trisphosphate
- Inositol Phosphates
(pharmacology)
- Ionomycin
- Membrane Potentials
(drug effects)
- Microinjections
- Neuroblastoma
(physiopathology)
- Sugar Phosphates
(pharmacology)
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