Tsai M C, Chen M L
Life Sci. 1987 Jun 8;40(23):2229-36. doi: 10.1016/0024-3205(87)90058-0.
The effects of phencyclidine(PCP) on the post-tetanic potentiation(PTP) of twitch tension were studied on the isolated mouse phrenic nerve diaphragm preparation. Phencyclidine increased directly elicited twitch tension while it decreased post-tetanic potentiation of the indirectly elicited twitch tension. The maximal depression effect of the PTP was found after higher frequencies and longer durations of stimulation. After repetitive stimulation, the amplitude of endplate potential was potentiated. Phencyclidine decreased the post-tetanic potentiation of the amplitude of endplate potential while the quantal content of the endplate potential was not affected. 4-Aminopyridine increased both directly and indirectly elicited twitch tension while it did not inhibit the post-tetanic potentiation of the twitch tension. It is concluded that phencyclidine suppressed the post-tetanic potentiation of the indirectly elicited twitch tension. The depressant effect may be mainly due to its effect on the acetylcholine receptor-ionic channel complex of the motor endplate.
在离体小鼠膈神经膈肌标本上研究了苯环己哌啶(PCP)对强直后增强(PTP)引起的肌肉收缩张力的影响。苯环己哌啶可直接增加诱发的肌肉收缩张力,同时降低间接诱发的肌肉收缩张力的强直后增强。在较高频率和较长刺激持续时间后发现PTP的最大抑制作用。重复刺激后,终板电位的幅度增强。苯环己哌啶降低了终板电位幅度的强直后增强,而终板电位的量子含量未受影响。4-氨基吡啶可直接和间接增加诱发的肌肉收缩张力,同时不抑制肌肉收缩张力的强直后增强。得出的结论是,苯环己哌啶抑制了间接诱发的肌肉收缩张力的强直后增强。其抑制作用可能主要归因于其对运动终板乙酰胆碱受体-离子通道复合物的作用。