Perney T M, Hirning L D, Leeman S E, Miller R J
Proc Natl Acad Sci U S A. 1986 Sep;83(17):6656-9. doi: 10.1073/pnas.83.17.6656.
We examined the effects of dihydropyridine drugs on evoked neurotransmitter release from cultured neonatal rat sensory and sympathetic neurons. Depolarization with K+-rich solutions increased the release of substance P from cultured sensory neurons. This release was enhanced by BAY K8644 and (+)-202791 and was blocked by a variety of other dihydropyridines including (-)-202791, by Co2+, or in Ca2+-free solutions. K+-rich solutions also stimulated the release of [3H]norepinephrine from cultured sympathetic neurons. This release was also completely blocked by Co2+ or in Ca2+-free solution. In contrast to the situation in sensory neurons, however, the evoked release of [3H]norepinephrine was completely resistant to the blocking effects of dihydropyridine such as nimodipine. However, BAY K8644 was able to enhance the evoked release of [3H]norepinephrine, and this enhancement was blocked by nimodipine. These results are discussed in relation to the possible participation of multiple types of calcium channels in the release of neurotransmitters.
我们研究了二氢吡啶类药物对培养的新生大鼠感觉神经元和交感神经元诱发神经递质释放的影响。用富含钾的溶液进行去极化可增加培养的感觉神经元中P物质的释放。BAY K8644和(+)-202791可增强这种释放,而包括(-)-202791在内的多种其他二氢吡啶、Co2+或在无钙溶液中可阻断这种释放。富含钾的溶液也可刺激培养的交感神经元释放[3H]去甲肾上腺素。这种释放在Co2+存在或无钙溶液中也被完全阻断。然而,与感觉神经元的情况不同,诱发的[3H]去甲肾上腺素释放对尼莫地平等二氢吡啶的阻断作用完全具有抗性。然而,BAY K8644能够增强诱发的[3H]去甲肾上腺素释放,且这种增强作用被尼莫地平阻断。结合多种类型钙通道可能参与神经递质释放的情况对这些结果进行了讨论。