Maloteaux J M, Octave J N, Laterre E C
Laboratoire de Neurochimie, Université Catholique de Louvain, Brussels, Belgium.
Neurosci Lett. 1988 Apr 22;87(1-2):168-72. doi: 10.1016/0304-3940(88)90164-4.
There is a high affinity binding of [3H]PN 200-110 (Kd = 0.21 nM) to slow calcium channels in cultured neurones. Several calcium antagonists, which recognize the [3H]PN 200-110 binding site, did not affect the K+-induced calcium uptake. The calcium channel activator BAY K 8644 increased the calcium uptake in depolarizing conditions and this effect was antagonized by pharmacological concentrations of calcium entry blockers. We conclude that the dihydropyridine binding site is involved in the modulation of calcium entry through the voltage-sensitive channel in depolarized cultured neurones.
[3H]PN 200 - 110(解离常数Kd = 0.21 nM)与培养神经元中的慢钙通道具有高亲和力结合。几种识别[3H]PN 200 - 110结合位点的钙拮抗剂并不影响钾离子诱导的钙摄取。钙通道激活剂BAY K 8644在去极化条件下增加了钙摄取,并且这种效应被药理学浓度的钙内流阻滞剂所拮抗。我们得出结论,二氢吡啶结合位点参与了去极化培养神经元中通过电压敏感通道的钙内流调节。