[calcium-induced calcium release: Ca2+-induced Ca2+ release]

カルシウム誘導性カルシウム放出。
初めBerridgeによって提唱された。

【機能】

　　・カルシウムシグナルを増幅
　　・カルシウム・ウェーブ

【機構】

　◆細胞内カルシウムストア（Fabiato & Fabiato, 1975）
　　・リアノジン受容体
　　　　Ca2+-sensitive ryanodine receptors (RyRs)
　　　　神経でもsmooth endoplasmic reticulum (ER) membraneに存在
　　・IP3受容体

【薬】

　◆阻害
　　・thapsigargin 1uM
　◆惹起
　　・caffeine

Calcium-induced calcium release regulates action potential generation in guinea-pig sympathetic neurones

　・筋で初め調べられた
　・神経でも生じる
　　　(Marrion&Adams,1992; Kuba,1994; Verkhratsky&Shmigol,1996;
　　　 Cohen,1997; Berridge,1998)
　・神経での機能
　　　（Kawai&Watanabe,1989; Sah&McLachlan,1991; Jobling,1993; Moore,1998)
　・mudpuppy parasympathetic neurones
　　　CICRは自発miniature外向き電流(SMOCs)活性化
　　　　BKチャネルが関与(Merriam,1999; Scornik,2001)
　　　心臓神経のランプに対する活動電位発生の潜時を調節(Parsons,2002)
　　　　ERのcaffeine-sensitive細胞内Ca2+ stores枯渇で消失
　　　　電位依存性Caチャネル抑制で消失
　　　　BKチャネルブロックで消失
　　　CICRでCa濃度局所的に>40uM(Scornik,2001) to activate membrane outward currents that decrease the effectiveness of the depolarizing current (Parsons et al. 2002).

These recent observations in amphibian autonomic neurones demonstrate a previously undefined role for CICR. CICR can act as an amplification mechanism for Ca2+, activating a subpopulation of BK channels, not directly activated by Ca2+ influx, that act to prolong the latency to AP generation. However, it has not been reported whether this regulatory role of CICR exists in mammalian autonomic neurones. The present study, in dissociated guinea-pig stellate sympathetic neurones, demonstrates that caffeine activates RyRs and causes a rise in [Ca2+]i, verifying the presence of CICR. Furthermore, pharmacological disruption of CICR decreased the latency to AP generation produced by depolarizing current ramps. These observations indicated that this novel CICR-mediated mechanism can regulate AP generation in guinea-pig sympathetic stellate neurones as well.