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マウス近位結腸における自発性電気活動の性質

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:
2019年
DOI:
10.1254/jpssuppl.92.0_1-O-10
会議属性:
国内会議
査読:
無し
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:
マウス近位結腸における自発性電気活動の性質
発表情報:
第92回日本薬理学会年会, 2019, 3, 14-16, 大阪 巻: 92 ページ: 1-O-10
キーワード:
概要:
Properties of spontaneous electrical activity in the mouse proximal colon were studied using intracellular recording. Spike complexes with a frequency of 1 ~ 3 cycles/min occurred in the longitudinal muscles. Each spike complex consisted of a burst of action potentials (APs) 15 ~ 35 mV in amplitude and 10 ~ 40 APs per complex. The resting membrane potentials were -40 ~ - 50 mV. Spike complexes were abolished by verapamil, a Ca2+ blocker, pinacidil, a KATP channel opener, NPPB, a Ca2+ - activated Cl- channel (CACC) blocker, and bumetanide, a Na+ - K+ - 2Cl- co-transporter (NKCC1) inhibitor. Spike complexes and spontaneous transient depolarizations (STDs) were recorded from myenteric interstitial cells of Cajal (ICC-MY). Spike complexes in ICC-MY were also abolished by verapamil, pinacidil, NPPB and bumetanide. The amplitude of STDs were inhibited by verapamil and NPPB, but increased by pinacidil. These results suggest that the activation of CACC is associated with the generation of spontaneous electrical activity in the mouse proximal colon. Since CACC and NKCC1 are expressed only in ICC-MY, spike complexes seem to be generated in ICC-MY and transferred to nearby smooth muscle layers electrotonically.
抄録:
プログラム, p176, 1-O-10

英語フィールド

Author:
Kito Y, Kurahashi M
Title:
Properties of spontaneous electrical activity in the mouse proximal colon.
Announcement information:
The 92nd Annual Meeting of the Japanese Pharmacological Society, 2019, 3, 14-16, Osaka Vol: 92 Page: 1-O-10
An abstract:
Properties of spontaneous electrical activity in the mouse proximal colon were studied using intracellular recording. Spike complexes with a frequency of 1 ~ 3 cycles/min occurred in the longitudinal muscles. Each spike complex consisted of a burst of action potentials (APs) 15 ~ 35 mV in amplitude and 10 ~ 40 APs per complex. The resting membrane potentials were -40 ~ - 50 mV. Spike complexes were abolished by verapamil, a Ca2+ blocker, pinacidil, a KATP channel opener, NPPB, a Ca2+ - activated Cl- channel (CACC) blocker, and bumetanide, a Na+ - K+ - 2Cl- co-transporter (NKCC1) inhibitor. Spike complexes and spontaneous transient depolarizations (STDs) were recorded from myenteric interstitial cells of Cajal (ICC-MY). Spike complexes in ICC-MY were also abolished by verapamil, pinacidil, NPPB and bumetanide. The amplitude of STDs were inhibited by verapamil and NPPB, but increased by pinacidil. These results suggest that the activation of CACC is associated with the generation of spontaneous electrical activity in the mouse proximal colon. Since CACC and NKCC1 are expressed only in ICC-MY, spike complexes seem to be generated in ICC-MY and transferred to nearby smooth muscle layers electrotonically.


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