| Project/Area Number |
09671731
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Otorhinolaryngology
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| Research Institution | Tohoku University |
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Principal Investigator |
KAWASE Tetsuaki Tohoku University, hospital, Department of Otolaryngology, Lecturer, 医学部・附属病院, 講師 (50169728)
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| Co-Investigator(Kenkyū-buntansha) |
HASHIMOTO Sho Tohoku University, School of Medicine, Department of Otolaryngology, Associate P, 医学部, 助教授 (20156285)
IKEDA Katsuhisa Tohoku University, School of Medicine, Department of Otolaryngology, Lecturer, 医学部, 講師 (70159614)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 1998: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1997: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | spiral ganglion / Ca^<2+> / hearing loss / LIVE and DEAD Viability / Cytotoxity Assay / Fluo-3 and Fura-Red / LASER-scanning microscope |
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| Research Abstract |
Intracellular Ca^<2+> plays an important role in the cellular functions of various tissues. In the spiral ganglion cells, neurotransmitter release is known to be dependent on cytosolic Ca^<2+> responses through voltage-dependent Ca^<2+> channels. We examined cytosolic Ca^<2+> responses induced by depolarization in the isolated spiral ganglion cells of the kanamycin-intoxicated guinea-pig to evaluate the activity of theCa^<2+> channel in pathological conditions.
Albino guinea-pigs (weight 250-250g) received intramuscular injections of 400 mg/kgkanamycin 5 times per week for 3 weeks. Guinea pigs without treatment were used as controls. Control guinea-pigs showed normal ABR responses. On the other hand, kanamycin-intoxicatedguinea pigs showed no detectable responses below 65 dB SPL evoked by click. Spiral ganglion cells of the guinea-pig cochlea were mechanically isolated. Dynamic changes in intracellular Ca^<2+>concentration were estimated with Fluo-3/Fura-Red ratiometric method using a LASER-scanning microscope. Activation of the Ca^<2+> channel was obtained by high K+-induced depolarization.
High K+-induced deporalization elevated the cytosolic Ca^<2+> concentration of the ganglion cells. Some of the cells showed oscillatory increases in the cytosolic Ca^<2+> level. Furthermore, the cytosolicCa^<2+> response induced by depolarization was decreased in damaged spiral ganglion cells compared with that in control cells.
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