1989 Fiscal Year Final Research Report Summary
Signal transduction and ionic movement of cell membrane
| Project/Area Number |
63304030
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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 | Nagoya University, School of Medicine |
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Principal Investigator |
TOMITA Tadao Nagoya Univ. Physiology Professor, 医学部, 教授 (50078763)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAGISHI Shunichi Okazaki Nat. Res. Inst. Professor, 生理学研究所, 教授 (70014032)
NOMA Akinori Kyushu Univ. Physiology Professor, 医学部, 教授 (00132738)
KUBA Kenji Saga Med. Sch. Physiology Professor, 医学部, 教授 (60080561)
AKASU Takashi Kurume Univ. Physiology Professor, 医学部, 教授 (60113213)
AKAIKE Norio Tohoku Univ. Path. Physiol. Professor, 医学部, 教授 (30040182)
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| Project Period (FY) |
1988 – 1989
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| Keywords | Ionic channel / Channel gating / Receptor / Cell membrane signaling / Second messenger / Ca-influx / Intracellular Ca / Neuronal differentiation |
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| Research Abstract |
In the process of reception of signals, cells generally increase the membrane permeability to various ions by opening ionic channels. Two categories of channels have been considered: one controlled by a gate which is sensitive to membrane potential and the other by a gate which is controlled by chemical processes, including binding of polyvalent cations,such as Ca^<2+>. Channels involved in permeability changes following receptor activation belong to the latter category.
In this research, we have investigated various channel properties in several cell types mainly employing electrophysiological techniques. The following are the main findings. Channel gating is affected by fatty acids and hydrophobic substances, probably by altering membrane fluidity. IntracellularCa seems to activate directly a K^+ channel and H^+ has blocking action on this channel. K^+ channels activated by external Ca^<2+> were found in a vascular muscle and Cl^- channels by internal Ca^<2+> in neurons. On the other hand, Cl^- channels activated through nicotinic and GABA receptors were inhibited by internal Ca^<2+>. In sympathetic ganglia, depolarization of the membrane increases Ca-influx and releases Ca^<2+> from intracellular stores. In these neurons, many second messengers (cyclic AMP, cyclic GMP) affect channels properties. These messengers may cause very prolonged effects on ionic channels. A close correlation was found between neural differentiation and the appearance of various types of ionic channels in the plasma membrane.
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