Woodward J J, Rezazadeh S M, Leslie S W
Division of Pharmacology, College of Pharmacy, University of Texas, Austin 78712.
Brain Res. 1988 Dec 13;475(1):141-5. doi: 10.1016/0006-8993(88)90207-7.
The presynaptic neurotoxin omega-conotoxin (omega-CgTx) was tested for its ability to inhibit voltage-dependent calcium flux and transmitter release in rat brain synaptosomes. Conotoxin (0.001-10 microM) had no effect on calcium uptake or endogenous dopamine release from rat striatal synaptosomes in the absence of potassium depolarization. Fast-phase potassium stimulated calcium influx was only partially (20-30%) inhibited by conotoxin at concentrations between 1 nM and 10 microM. The fast-phase release of endogenous dopamine from the same synaptosomal preparation was inhibited by approximately 25% at 0.01 microM and by 60% at 10 microM. These results suggest that a subgroup of high affinity omega-CgTx-sensitive calcium channels may be involved in regulating the release of endogenous dopamine from brain synaptosomes.
对突触前神经毒素ω-芋螺毒素(ω-CgTx)抑制大鼠脑突触体中电压依赖性钙通量和递质释放的能力进行了测试。在无钾去极化的情况下,芋螺毒素(0.001 - 10微摩尔)对大鼠纹状体突触体的钙摄取或内源性多巴胺释放没有影响。在1纳摩尔至10微摩尔的浓度范围内,快速相钾刺激的钙内流仅被芋螺毒素部分抑制(20 - 30%)。来自相同突触体制备物的内源性多巴胺的快速相释放,在0.01微摩尔时被抑制约25%,在10微摩尔时被抑制60%。这些结果表明,一组高亲和力的ω-CgTx敏感钙通道可能参与调节脑突触体中内源性多巴胺的释放。