日本生理学会大会発表要旨集
日本生理学会大会発表要旨集
セッションID: 1P014
会議情報
Cellular & molecular physiology
ホスホリパーゼC連関受容体アゴニストおよびSERCA阻害剤によって引き起こされる容量性カルシウム流入活性化機構の相違
尾松 万里子藤居 祐介松浦 博
著者情報
会議録・要旨集 フリー

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抄録
Stimulation of phospholipase C-coupled receptor induces a release of Ca2+ from the intracellular stores and subsequent influx of Ca2+ across the plasma membrane, termed store-operated Ca2+ entry (SOCE). SOCE is also induced by inhibition of sarcoplasmic endoplasmic reticulum Ca2+ pump (SERCA). One of the hypothesized mechanisms by which the state of filling of the stores is communicated to the plasma membrane is direct or indirect association of two membranes. Noradrenaline is known to induce a rapid [Ca2+]i increase followed by the activation of SOCE in brown adipocytes. To investigate spatial changes in [Ca2+]i during the activation of SOCE, confocal line scanning of [Ca2+]i was performed in fluo-3-loaded rat brown adipocytes. Linescan images were acquired by repeatedly scanning the laser beam along with a single line at 5-200 msec intervals. When the cells were exposed to 1 μM noradrenaline, rapid [Ca2+]i increase was observed in intracellular space in close vicinity to the plasma membrane followed by the increase in whole cytoplasmic space, indicating the possibility that ER locate close to the plasma membrane. On the other hand, SERCA inhibitor thapsigargin (100 nM) firstly induced a slower rise in the central area distanced from the plasma membrane followed by the gradual spreading of Ca2+ increase in whole cytoplasmic space. These results suggest that the activation mechanism of SOCE induced by noradrenaline is different from that induced by thapsigargin. [Jpn J Physiol 55 Suppl:S71 (2005)]
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© 2005 日本生理学会
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