1987 Fiscal Year Final Research Report Summary
Ion Channel and Cellular Metabolism
| Project/Area Number |
61304031
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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 | Shiga University of Medical Science |
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Principal Investigator |
KITASATO Hiroshi Shiga University of Medical Science, Professor, 医学部, 教授 (20079700)
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| Co-Investigator(Kenkyū-buntansha) |
TONOSAKI Akira Yamagata University, School of Medicine, Professor, 医学部, 教授 (90004572)
TAKAHASHI Kunitarou Faculty of Medicine, University of Tokyo, Professor, 医学部, 教授 (10010034)
TOMITA Tadao Nagoya University, School of Medicine, Professor, 医学部, 教授 (50078763)
KUBA Kenji Saga Medical School,Professor, 医学部, 教授 (60080561)
NORIO Akaike Faculty of Medicine, Kyushu University, Associate Professor, 医学部, 助教授 (30040182)
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| Project Period (FY) |
1986 – 1987
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| Keywords | Ca^<2+>-activated K^+-channel / Cl^--channel / dorsal root ganglion cell / squid giant axon / pancreatic B cell / glutamate receptor / JSTX / IAP |
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| Research Abstract |
The gating mechanism of ion channel has been mainly studied in terms of voltage-dependency and transmitter-dependency. Recent development of technique to investigate ion channels has made it possible to elucidate the relationship between the activity of ion channels and the intracellular metabolism. Present research was conducted in three different levels; the development of new technique and the more precise examination on channel property, the modulation of channel activity by intracellular substances, and the cellular differentiation and growth. During the project term we had a meeting two times to discuss the newly obtained experimental results with researchers who were interested in the progress in the field. Main results of present research are as follows:
A new intracellular perfusion technique with oil-gap was developed. One end of a cell was cut in a pool separated by a oil-gap from another pool. Through the cut end the internal solution of the cell was rapidly changed. The kinetic properties of Ca^<2+>-activated K^+-channels were precisely studied in experiments of simulatneous measurements of patch-clamp current and Fura 2 fluorescence. From these studies Ca^<2+>-activated K^+-channels were classified into three groups. Important findings were obtained from experiments on Cl^--channels also. Lowering the internal Ca^<2+> concentration to 10^<-10> M caused an increase in Cl^- permeability in squid giant axons. In frog dorsal root ganglion cell, a suppression of Cl^- current by increasing internal Ca^<2+> was found. A novel glutamate receptor was found in presynaptic fiber of lobster. Stimulating the glutamate receptor caused an increase of K^+ permeability. The effect of glutamate on K^+ permeability was not blocked by JSTX, but suppressed by IAP. A new technique of tissue culture was developed. The technique was based on the observation that neurons in culture medium extended their axon along artificially etched narrow grooves.
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