Pileblad E, Carlsson A
Neuropharmacology. 1987 Jan;26(1):101-5. doi: 10.1016/0028-3908(87)90052-9.
The effects of the Ca++-antagonist nimodipine and the Ca++-agonist Bay K 8644 on brain catecholamine synthesis in male albino mice were investigated in vivo. Nimodipine caused a dose-dependent reduction in the synthesis rate of dopamine and noradrenaline, measured as the accumulation of 3,4-dihydroxyphenylalanine (DOPA) after inhibition of the L-aromatic amino acid decarboxylase with 3-hydroxybenzylhydrazine (NSD 1015). In contrast, Bay K 8644 caused an increase in DOPA synthesis. Furthermore, Bay K 8644 dose-dependently antagonized the effect of nimodipine. It is suggested that nimodipine and Bay K 8644 induced these changes by interfering with neuronal Ca++ transport, thus arguing for a role of voltage operated Ca++ channels in normal nerve function.
在雄性白化小鼠体内研究了钙离子拮抗剂尼莫地平和钙离子激动剂Bay K 8644对脑内儿茶酚胺合成的影响。用3-羟基苄基肼（NSD 1015）抑制L-芳香族氨基酸脱羧酶后，以3,4-二羟基苯丙氨酸（DOPA）的积累量来衡量，尼莫地平导致多巴胺和去甲肾上腺素的合成速率呈剂量依赖性降低。相反，Bay K 8644导致DOPA合成增加。此外，Bay K 8644呈剂量依赖性地拮抗尼莫地平的作用。提示尼莫地平和Bay K 8644通过干扰神经元钙离子转运诱导了这些变化，因此表明电压门控钙离子通道在正常神经功能中起作用。
