1999 Fiscal Year Final Research Report Summary
Protein kinase activation enhances neuronal excitability by increasing persistent NaィイD1+ィエD1
| Project/Area Number |
10680754
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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 |
Neuroscience in general
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| Research Institution | Fujita Health University |
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Principal Investigator |
HIDAKA Soh Fujita Health Univ., Sch. Med., Physiol.., Associate Professor, 医学部, 講師 (00228735)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAUCHI Masamitsu Aichi Gakusen Coll., Nutrition & Food Sciences, Assistant Professor, 生活科, 講師 (30278303)
MIYACHI Ei-ichi Fujita Health Univ., Sch. Med., Physiol..,Chairman, 医学部, 教授 (90129685)
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| Project Period (FY) |
1998 – 1999
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| Keywords | synaptic plasticity / action potential / voltage-gated Na+ channels / gap junctions / protein kinases / protein phosphoraylatin / retina / patch-clamp methods |
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| Research Abstract |
Retinal ganglion cell (RGCs) encode the input our brains use to sense visual information in the retina. RGCs extract this information from synapses of bipolar and amacrine cells in the inner plexiform layer, and transform it into spike trains in the optic nerve. To know which inputs control specific properties of synaptic outputs from RGCs, it is necessary to investigate how RGCs generate action potentials (APs). Voltage-gated NaィイD1+ィエD1 currents are responsible for generation of APs from RGCs. Functional modulation of voltage-gated NaィイD1+ィエD1 channels in RGCs would be expected to influence the encoding of visual information into the spike trains. We have first examined phosphorylation of ion channel proteins by activation of neurotransmitter receptors coupled to activation of protein kinases with biochemical techniques. Secondly, we have investigated the effects of protein kinase activation on whole-cell NaィイD1+ィエD1 currents and generation of APs in RGCs, using amphotericin-B-perfor
… More
ated patch-clam methods. Biochemical experiments revealed that ion channels were phosphorylated by activation of protein kinases and dephosphorylated by activation of protein phosphatases. Voltage-clamp experiments showed that two components of NaィイD1+ィエD1 currents appear to be activated by depolarizations ; e.g.. a trasient component followed by a persistent component, under control conditions. Activation of protein kinase A decreased the amplitude of the maximal transient current, and slowed its decay without markedly altering the voltage-dependence of current activation. It also increased the amplitude of persistent NaィイD1+ィエD1 current. Current clamp experiments indicated that activation of protein kinase A enhanced neuronal excitability by inducting a decrease in voltage threthold for generation of APs and caused an increase in spike frequency from RGCs. Since persistent NaィイD1+ィエD1 current sets the threthold for generation of APs, an increase in persistent Na+ current must lead to a marked increase in repetitive firing of spikes from RGCs. The present study suggest that phosphorylation of Na+ channels by activation of protein kinase A enhances the encoding of visual information into the spike trains from RGCs via an increase in persistent Na+ current at functional critical subthrethold voltages. This novel effect would be included in synaptic plasticity for generation of APs in RGCs. Less
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[Publications] Hidaka, S., Yamauchi, M., Nishikawa, C., Kato, T. and Miyachi, E.-I.: "Gap junction channels, connexin43, of rat retinal pigment epithelial cells"Society of Neuroscience Abstract. 25. 134 (1999)
Description
「研究成果報告書概要(和文)」より
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