Olivier V, Miquet J M, Aubeneau M, Blanchard J C, Doble A, Boireau A
Rhône-Poulenc Rorer S.A., Centre de Recherche de Vitry-Alfortville, Département Biologie, Vitry-sur-Seine, France.
J Pharm Pharmacol. 1992 Jan;44(1):61-3. doi: 10.1111/j.2042-7158.1992.tb14366.x.
The effects of veratridine-induced depolarization on [3H]dopamine ([3H]DA) release in the presence of a physiological (5 mM) or a depolarizing (25 mM) concentration of K+ were studied in-vitro in rat superfused striatal ribbons. A combination of the two depolarizing agents induced a marked potentiation in the overflow of [3H]DA, giving an overall 3- to 5-fold increase in veratridine activity. This potentiation was completely antagonized by tetrodotoxin (100 nM). These studies indicated that K(+)-induced depolarization can increase the potency of veratridine in releasing dopamine from terminals.
在体外对大鼠灌流纹状体条带进行研究，观察在生理浓度（5 mM）或去极化浓度（25 mM）的钾离子存在下，藜芦碱诱导的去极化对[3H]多巴胺（[3H]DA）释放的影响。两种去极化剂联合使用可显著增强[3H]DA的溢出，使藜芦碱活性总体增加3至5倍。这种增强作用可被河豚毒素（100 nM）完全拮抗。这些研究表明，钾离子诱导的去极化可增强藜芦碱从神经末梢释放多巴胺的能力。
