Tokumaru H, Satoh Y, Hirashima N, Shojaku S, Yamamoto H, Kirino Y
Faculty of Pharmaceutical Sciences, University of Tokyo, Japan.
Biol Pharm Bull. 1997 Jun;20(6):641-5. doi: 10.1248/bpb.20.641.
The high K(+)-evoked release of acetylcholine (ACh) from electric organ synaptosomes isolated from the Japanese marine ray, Narke japonica, was strongly inhibited by dihydropyridines at micromolar concentrations. However, this inhibition seems to be a non-specific effect since the agonist (-)-Bay K 8644 also had inhibitory effects. Calciseptine, a peptide toxin specific for L-type Ca channels, inhibited to a lesser extent the evoked acetylcholine release: the maximum inhibition was about 20%. This finding is in accord with our data (Tokumaru et al., J. Neurochem., 65, 831(1995)) regarding inhibition by a monoclonal antibody against the alpha 2 delta-subunit of the L-type Ca channel and provides evidence for the involvement of an L-type-like Ca channel in ACh release in addition to omega-conotoxin GVIA-sensitive N-type and omega-agatoxin IVA-sensitive P-type Ca channels.
从日本海产电鳐(Narke japonica)分离出的电器官突触体中,高钾诱发的乙酰胆碱(ACh)释放受到微摩尔浓度二氢吡啶的强烈抑制。然而,这种抑制似乎是非特异性的,因为激动剂(-)-Bay K 8644也有抑制作用。钙抑素是一种对L型钙通道具有特异性的肽毒素,对诱发的乙酰胆碱释放的抑制作用较小:最大抑制率约为20%。这一发现与我们的数据(Tokumaru等人,《神经化学杂志》,65,831(1995))一致,该数据涉及针对L型钙通道α2δ亚基的单克隆抗体的抑制作用,并为除ω-芋螺毒素GVIA敏感的N型和ω-阿加毒素IVA敏感的P型钙通道外,类似L型的钙通道参与乙酰胆碱释放提供了证据。