1993 Fiscal Year Final Research Report Summary
A study on the mechanism of intracellular Ca^<2+> release in neurones and its physiological functions.
| Project/Area Number |
04454139
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
神経・筋肉生理学
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| Research Institution | Saga Medical School |
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Principal Investigator |
KUBA Kenji Saga Medical School, Physiology, Professor, 医学部, 教授 (60080561)
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| Co-Investigator(Kenkyū-buntansha) |
NOHMI Mitsuo Saga Medical School, Center for M.S.R.E, Associate Professor, 医学部, 助教授 (80117209)
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| Project Period (FY) |
1992 – 1993
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| Keywords | Intracellular Ca^<2+> / Ca^<2+> -induced Ca^<2+> release / Ca^<2+> influx / Bullfrog sympathetic ganglion cells / Rabbit otic ganglion cells / Cylic ADP-ribose / Mitochondria Cyclosporin-A / サイクロスポリンA |
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| Research Abstract |
The mechanism of intracellular Ca^<2+> release and its physiological functions were studied in cultured bullfrog sympathetic and rabbit otic ganglion cells, using fura-2 or indo-1 fluorescence redording techniques with a photomultiplier or confocal laser-scanning microscope and shole cell patch clamp techniques. Ryanodine-sensitive Ca^<2+> -induced Ca^<2+> release (CICR) in bullfrog sympathetic neurones were voltage-dependently activated throughout the cytoplasm by Ca^<2+> influx produced by a depolarizing voltage pulse (> 100 ms), but only in the submembrane regions by Ca^<2+> influx caused by action potentials (> 10 Hz, 100 pulses). Under the effects of intracellular cyclic ADP-ribose, tetanic action potentials activated propagating CICR.
iIn cultured rabbit otic ganglion cells, when the extracellular Ca^<2+> was reduced to a level < 0.1 mM, a small Ca^<2+> entry produced by a high K^+ -induced depolarization caused a propagating Ca^<2+> release from mitochondria which was blocked by cyclosprin A.
These two mechanisms may operate in ceurones in situ depending on the extracellular Ca^<2+> levels that would be altered by activities of neighboring neurones.
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