Martin-Moutot N, Seagar M, Couraud F
Laboratoire de Biochimie, INSERM U 172, CNRS URA 1179, Faculté de Médecine Nord, Marseilles, France.
Neurosci Lett. 1990 Jul 31;115(2-3):300-6. doi: 10.1016/0304-3940(90)90472-l.
Subtypes of voltage-sensitive calcium channels have been investigated in cultured rat brain neurons using two classes of specific probes, dihydropyridine compounds and omega-conotoxin. Membranes prepared from cultured neurons contain specific binding sites for [3H]PN200-110, a dihydropyridine antagonist, and for 125I-omega-conotoxin with a stoichiometry of about 1:1. A depolarization induced 45Ca2+ influx into intact brain neurons was partially inhibited by a dihydropyridine antagonist, nifedipine and stimulated by a dihydropyridine agonist, Bay K8644. This dihydropyridine sensitive 45Ca2+ flux was insensitive to omega-conotoxin at concentrations which saturate the specific toxin binding sites indicating that in cultured brain neurons, dihydropyridine-sensitive calcium channels are not sensitive to omega-conotoxin.
利用两类特异性探针，即二氢吡啶化合物和ω-芋螺毒素，对培养的大鼠脑神经元中的电压敏感性钙通道亚型进行了研究。从培养的神经元制备的膜含有[3H]PN200-110（一种二氢吡啶拮抗剂）和125I-ω-芋螺毒素的特异性结合位点，化学计量比约为1:1。去极化诱导45Ca2+流入完整的脑神经元，部分被二氢吡啶拮抗剂硝苯地平抑制，并被二氢吡啶激动剂Bay K8644刺激。这种对二氢吡啶敏感的45Ca2+通量在使特异性毒素结合位点饱和的浓度下对ω-芋螺毒素不敏感，表明在培养的脑神经元中，对二氢吡啶敏感的钙通道对ω-芋螺毒素不敏感。
