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一般演題(口頭)交感神経によるマウス結腸運動制御機構

発表形態:
一般講演(学術講演を含む)
主要業績:
主要業績
単著・共著:
共著
発表年月:
DOI:
10.1254/jpssuppl.95.0_2-O-093
会議属性:
国内会議
査読:
有り
リンク情報:

日本語フィールド

著者:
鬼頭 佳彦, 倉橋 正明
題名:
一般演題(口頭)交感神経によるマウス結腸運動制御機構
発表情報:
第95回日本薬理学会年会(ハイブリッド開催), 2022, 3, 7-9(On-Site及びRemote開催) 巻: 95 ページ: 2-O-093-
キーワード:
colon, adrenergic alpha receptor, smooth muscle
概要:
Morphological study revealed that sympathetic neurons are closely associated with PDGFRα + cells in mouse colonic musculature. In addition, gene expression study showed that α1A adrenoceptors (α1A ARs) are expressed exclusively in PDGFRα + cells of mouse colon. Therefore, we investigated how sympathetic neurons regulate mouse colonic motility via α1A ARs in PDGFRα + cells. Noradrenaline (NAd), via α1A ARs, activated a small conductance Ca2+-activated K+ (SK) channels and hyperpolarized a single PDGFRα + cell (the α1A AR ? SK channel signal pathway), resulting in hyperpolarization of neighboring smooth muscle cells (SMCs) connected by gap junctions, leading to inhibition of spontaneous contractions of colonic muscle. Sympathetic nerve stimulation (SNS) inhibited propulsive contractions represented by the colonic migrating motor complexes (CMMCs) via the α1A AR ? SK channel signal pathway in wild type mouse, however CMMCs were not affected by SNS in the colon of Adra1a?/? mouse. These results suggest that NAd released from sympathetic neurons inhibited mouse colonic motility via the α1A AR ? SK channel signal pathway in PDGFRα + cells.
抄録:
日本薬理学会年会要旨集, 95, 2-O-093

英語フィールド

Author:
Yoshihiko Kito, Masaaki Kurahashi
Title:
Oral Sessions Sympathetic neuronal mechanisms in the regulation of mouse colonic motility
Announcement information:
The 95th Annual Meeting of the Japanese Pharmacological Society, 2022, 3, 7-9(On-Site or Remote event) Vol: 95 Page: 2-O-093-
Keyword:
colon, adrenergic alpha receptor, smooth muscle
An abstract:
Morphological study revealed that sympathetic neurons are closely associated with PDGFRα + cells in mouse colonic musculature. In addition, gene expression study showed that α1A adrenoceptors (α1A ARs) are expressed exclusively in PDGFRα + cells of mouse colon. Therefore, we investigated how sympathetic neurons regulate mouse colonic motility via α1A ARs in PDGFRα + cells. Noradrenaline (NAd), via α1A ARs, activated a small conductance Ca2+-activated K+ (SK) channels and hyperpolarized a single PDGFRα + cell (the α1A AR ? SK channel signal pathway), resulting in hyperpolarization of neighboring smooth muscle cells (SMCs) connected by gap junctions, leading to inhibition of spontaneous contractions of colonic muscle. Sympathetic nerve stimulation (SNS) inhibited propulsive contractions represented by the colonic migrating motor complexes (CMMCs) via the α1A AR ? SK channel signal pathway in wild type mouse, however CMMCs were not affected by SNS in the colon of Adra1a?/? mouse. These results suggest that NAd released from sympathetic neurons inhibited mouse colonic motility via the α1A AR ? SK channel signal pathway in PDGFRα + cells.


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