| Project/Area Number |
02304031
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| Research Category |
Grant-in-Aid for Co-operative Research (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
General physiology
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| Research Institution | Saga Medical School |
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Principal Investigator |
KUBA Kenji Saga Medical School, Dept. Med., Prof., 医学部, 教授 (60080561)
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| Co-Investigator(Kenkyū-buntansha) |
TOMITA Tadao Nagoya, University, Dept. Med. Prof., 医学部, 教授 (50078763)
OKADA Yasunobu Kyoto University, Dept. Med., Recturer, 医学部, 講師 (10025661)
AKAIKE Norio Tohoku University, Dept. Med., Prof., 医学部, 教授 (30040182)
NOMA Akinori Kyushu University, Dept. Med., Prof., 医学部, 教授 (00132738)
TAKAHASHI Kunitaro University of Tokyo, Dept. Med., Prof., 医学部, 教授 (10010034)
赤須 崇 久留米大学, 医学部, 教授 (60113213)
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| Project Period (FY) |
1990 – 1991
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| Project Status |
Completed (Fiscal Year 1991)
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| Budget Amount *help |
¥10,300,000 (Direct Cost: ¥10,300,000)
Fiscal Year 1991: ¥5,400,000 (Direct Cost: ¥5,400,000)
Fiscal Year 1990: ¥4,900,000 (Direct Cost: ¥4,900,000)
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| Keywords | Excitable membranes / Ion channel / Modulator / Transmitter / Intracellular Ca^<2+> / Kinase / Second messenger / Neural differentiation / 急速外液交換技術 / 共焦点顕微鏡 / 骨奮性細胞 / イオン透過 / イオンチャネルの開閉制御 |
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| Research Abstract |
In regard to the mechanisms of modulation of ion permeation across the cell membrane, following specific problems were studied on a variety of cell type by eighteen investigators, and the results were obtained as follows. 1) Gating mechanism of ion channels : Activtion of Cl^- channels by Ca^<2+> or F^- in squid giant axons (Yamagishi), blockade of Na^+ channels by grayanotoxin and G-cyclam in giant axons (Seyama), activation and/or blockade by Na^+ and Mg^<2+> of Na^+-dependent K^+ channels in guinea-pig cardiac muscles (Noma), blockade of ACh receptor channels and enhancement of its de ensitization by diltiazem (Takeuchi), charge-transfer mechanism between Ca^<2+> channel at the t-tubule membran and Ca^<2+>-release channel at the sarccoplasmic reticulum (Inoue) and voltage-dependent Ca^<2+>-induced Ca^<2+> release mechanis m in bullfrog sympathetic neurones were found or analyzed. 2) Modulation of ion channel activities by transmitter and intracellular substances : Activation of Cl^-
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channel by cyclic AMP and Ca^<2+> in intestine epithelial cells (Okada), modulation of K^+ channels by Ca^<2+> and H^+ in pancreatic B cells (Kitasato), regulation of Ca^<2+> and K^+ channels by intracellular ATP and H^+ in smooth muscles (Tomita), biomodal modulation of NMDA-receptor channel by acetylcholine in Meynerte nucleus neurones (Akaike), activation by Ca^<2+> calmoduline-dependent kinase and inactivation by C-kinase of M-current in bullfrog sympathetic neurones (Akasu), phosphorylation of proteins by muscarine and cyclic GMP in rabbit sympathetic neurones (Kobayashi) were found or analyzed. 3) Neural differentiation and the regulation of ion channel expression : The regulatory mechanisms of gap junction channel expression during neural and epithelial inductions in ascidian embryos were claified (Takahashi). Culturing methods for analysis of synaptogenesis were developed (Fukuda). 4) Problems regarding axonal conduction : Inhibition of an axonal transport by acetylcholine (Takenaka), distribution and characteristics of cell membrane particles representing gap-junction channels and transmitter receptors in sympathetic ganglion cells and horizontal cells (Tonosaki) and optical properties of ion channels or related molecules during conduction in crayfish muscles (Watanabe) were found or analyzed. A new method for demonstration of three-dimensional structure of a neurone tree was developed (Koike). Less
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