| Project/Area Number |
06680758
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Neurochemistry/Neuropharmacology
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| Research Institution | Gifu University |
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Principal Investigator |
TAKEUCHI Hiroshi Gifu University School of Medicine, Physiology, Professor, 医学部, 教授 (10033333)
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| Co-Investigator(Kenkyū-buntansha) |
TONOSAKI Ken-ichi Laboratory of Physiology, Division of Veterinary Medicine, Gifu University, Facu, 農学部, 教授 (30103485)
YAMAMOTO Noriko Gifu University college of Medical Sciences, Professor, 医療技術短期大学部, 教授 (70021409)
ARAKI Yoko Gifu University School of Medicine, Physiology, Assistant Professor, 医学部, 助手 (20176374)
LEE Ken Gifu University School of Medicine, Physiology, Associate Professor, 医学部, 助教授 (00212316)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 1995: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1994: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | Signal transduction / Achatin-I / Neuropeptide / D-Amino acid / Voltage clamp / Molluscan giant neurone |
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| Research Abstract |
The effect of intracellular signal transduction system inhibitors on the inward current (I_<in>) caused by achatin-I,an Achatina endogenous tetrapeptide having a D-phenylalanine residue, applied locally onto the neurone tested, were examined under voltage clamp using two identifiable Achatina giant neurone types, v-RCDN and PON.H-89 (PKA inhibitor) markedly suppressed the achatin-I-induced I_<in> on PON, whereas this drug was ineffective on the I_<in> of v-RCDN.Dose (pressure duration)-response study of achatin-I on PON in a physiological solution and in the presence of H-89, and Lineweaver-Burk plot of these data, indicated that H-89 inhibited the I_<in> in noncompetitive manner. KT5823 (PKG inhibitor) suppressed the achatin-I-induced I_<in> of v-RCDN in mainly noncompetitive and partly uncompetitive manners, but this drug had no effect on the I_<in> of PON.W-7 (calmodulin inhibitor) suppressed noncompetitively the I_<in> of PON,but this drug had no effect on the I_<in> of v-RCDN.IBMX (cyclic nucleotide phophodiesterase inhibitor) enhanced the achatin-I-induced I_<in> of v-RCDN,but this drug was ineffective on the I_<in> of PON.However, IBMX might have effects on the achatin-I receptor sites on v-RCDN.These findings suggest multiple intracellular signal transduction pathways mediating the achatin-I-induced I_<in> : the I_<in> of PON is via PKA and probably Ca^<2+>/calmodulin-dependent protein kinase, and the I_<in> of v-RCDN via PKG.Other signal transduction system inhibitors including calphotin C (PKC inhibitor) did not significantly affect the I_<in> of both v-RCDN and PON.
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