Martin P, Laurent S, Massol J, Childs M, Puech A J
Département de Pharmacologie, Faculté de Médecine Pitié-Salpêtrière, Paris, France.
Eur J Pharmacol. 1989 Mar 14;162(1):185-8. doi: 10.1016/0014-2999(89)90620-1.
The present study was undertaken in order to determine the effects of the dihydropyridine calcium channel blocker, nimodipine and the dihydropyridine calcium channel activator BAY k 8644, in the learned helplessness test in the rat. Nimodipine dose dependently (0.5-2 mg/kg per day) reversed the behavioral deficit induced by inescapable shocks. The reversal of helpless behavior by imipramine (32 mg/kg per day) was antagonized by BAY k 8644 (0.5 and 1 mg/kg per day), and the effects of imipramine 8 and 16 mg/kg per day) were potentiated by a subeffective dose (0.5 mg/kg per day) of nimodipine. These results suggest that central dihydropyridine binding sites may be specifically involved in the modulation of the imipramine reversal of helpless behavior and favor a physiological role for dihydropyridine binding sites in the brain.
本研究旨在确定二氢吡啶类钙通道阻滞剂尼莫地平和二氢吡啶类钙通道激活剂BAY k 8644在大鼠习得性无助试验中的作用。尼莫地平剂量依赖性地（每天0.5 - 2毫克/千克）逆转了不可逃避电击诱导的行为缺陷。丙咪嗪（每天32毫克/千克）对无助行为的逆转作用被BAY k 8644（每天0.5和1毫克/千克）拮抗，而丙咪嗪（每天8和16毫克/千克）的作用被亚有效剂量（每天0.5毫克/千克）的尼莫地平增强。这些结果表明，中枢二氢吡啶结合位点可能特别参与丙咪嗪对无助行为逆转的调节，并支持二氢吡啶结合位点在大脑中的生理作用。
