WEKO3
アイテム
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Lambert-Eaton syndrome antibodies inhibit acetylcholine release and P/Q-type Ca2+ channels in electric ray nerve endings
http://hdl.handle.net/2261/1133
http://hdl.handle.net/2261/11331fe85ce3-0f1c-4c17-b103-ea8313413360
名前 / ファイル | ライセンス | アクション |
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427.pdf (995.5 kB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2016-12-13 | |||||
タイトル | ||||||
タイトル | Lambert-Eaton syndrome antibodies inhibit acetylcholine release and P/Q-type Ca2+ channels in electric ray nerve endings | |||||
言語 | ||||||
言語 | eng | |||||
キーワード | ||||||
主題 | MYASTHENIC SYNDROME ANTIBODIES | |||||
主題Scheme | Other | |||||
キーワード | ||||||
主題 | PRESYNAPTIC CALCIUM CHANNELS | |||||
主題Scheme | Other | |||||
キーワード | ||||||
主題 | OMEGA-CONOTOXIN | |||||
主題Scheme | Other | |||||
キーワード | ||||||
主題 | TRANSMITTER RELEASE | |||||
主題Scheme | Other | |||||
キーワード | ||||||
主題 | CHOLINERGIC SYNAPTOSOMES | |||||
主題Scheme | Other | |||||
キーワード | ||||||
主題 | NEUROMUSCULAR-JUNCTION | |||||
主題Scheme | Other | |||||
キーワード | ||||||
主題 | NARKE-JAPONICA | |||||
主題Scheme | Other | |||||
キーワード | ||||||
主題 | CURRENTS | |||||
主題Scheme | Other | |||||
キーワード | ||||||
主題 | ORGAN | |||||
主題Scheme | Other | |||||
キーワード | ||||||
主題 | CELLS | |||||
主題Scheme | Other | |||||
資源タイプ | ||||||
資源 | http://purl.org/coar/resource_type/c_6501 | |||||
タイプ | journal article | |||||
著者 |
Satoh, Yasushi
× Satoh, Yasushi× Hirashima, Naohide× Tokumaru, Hiroshi× Takahashi, Masanori P.× Kang, Jin× Viglione, Michael P.× Kim, Yong I.× Kirino, Yutaka |
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著者別名 | ||||||
識別子 | 2919 | |||||
識別子Scheme | WEKO | |||||
姓名 | 桐野, 豊 | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | The types of voltage-dependent calcium channels (VDCCs) present in the cholinergic terminals isolated from the electric organ of the ray, Narke japonica, were characterized on the basis of their pharmacological sensitivity to specific antagonists. Inhibition of these channel types by autoantibodies from patients with the Lambert-Eaton syndrome (LES) was then studied to determine the specificity of the pathogenic IgG. In normal untreated synaptosomal preparations, maximal doses of N- and P and/or Q-type Ca2+ channel antagonists, -conotoxin GVIA and -agatoxin IVA, inhibited depolarization-evoked ACh release by 47 % and 43 %, respectively. Calciseptine, an L-type VDCC antagonist, caused a 20 % reduction in the release. This indicates that the exocytotic release process is predominantly mediated by N- and P/Q-type VDCCs. LES IgG or sera caused an inhibition of ACh release by 39-45 % in comparison with the control antibody-treated preparations. The ionomycin-induced ACh release, however, was not altered by the antibodies. Additionally, the same LES antibodies inhibited whole-cell calcium currents (ICa) in bovine adrenal chromaffin cells. Thus, the pathogenic antibodies exert their action on VDCCs present in the synaptosomes. The efficacy of three Ca2+ channel antagonists in blocking ACh release was determined in preparations pretreated with LES IgG. -Agatoxin IVA produced only an additional 3-5 % reduction in release beyond that obtained with LES antibodies. Despite the pretreatment with LES IgG, -conotoxin GVIA and calciseptine inhibited the release to nearly their control levels. These results indicate that LES antibodies mainly downregulate P/Q-type Ca2+ channels which contribute to presynaptic transmitter release from the cholinergic nerve terminals of electric organ. The present findings are consistent with the hypothesis that P/Q-type VDCCs at the neuromuscular junction are the target of LES antibodies and that their inhibition by the antibodies produces the characteristic neuromuscular defect in this disease. | |||||
書誌情報 |
The Journal of physiology 巻 508, 号 2, p. 427-438, 発行日 1998-04-15 |
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ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 00223751 | |||||
書誌レコードID | ||||||
収録物識別子タイプ | NCID | |||||
収録物識別子 | AA00253169 | |||||
権利 | ||||||
権利情報 | © Copyright 1998 The Physiological Society | |||||
日本十進分類法 | ||||||
主題 | 491.37 | |||||
主題Scheme | NDC | |||||
出版者 | ||||||
出版者 | Cambridge University Press |