Effects of calcium channel blockers on stimulation-induced changes in transmitter release at the frog neuromuscular junction.
Effects of calcium channel blockers on stimulation-induced changes in transmitter release at the frog neuromuscular junction.
复制标题
钙通道阻滞剂对刺激引起的青蛙神经肌肉接头递质释放变化的影响。
DOI:
10.1002/syn.890150402
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发表时间:
1993
期刊:
影响因子:
--
通讯作者:
Mosier,DR
中科院分区:
文献类型:
--
作者:
Zengel,JE;Lee,DT;Sosa,MA;Mosier,DR
We have examined the effects of various calcium channel blockers on stimulation‐induced changes in end‐plate potential (EPP) amplitude at the frog neuro‐muscular junction. We found that the addition of small concentrations (1–10 μM) of Cd2+to the low calcium bathing Ringer reduced both the control EPP amplitude and the increase in EPP amplitude that normally occurs during repetitive stimulation under low quantal conditions. These effects of Cd2+, which developed rapidly following its addition to the bathing solution and were equally rapidly reversed, resulted from changes in the amount of transmitter released from the nerve terminal. The major effect of Cd2+appeared to be on the facilitation and augmentation components of increased release. Cd2+had little or no effect on potentiation of release. The other divalent cations tested, Zn2+, Co2+, and Ni2+, also decreased both control EPP amplitude and the stimulation‐induced increase in EPP amplitude, but higher concentrations (>100 μM) of these cations were required. The order of effectiveness in reducing stimulation‐induced increases in EPP amplitude was: Cd2+>>> Co2+, Zn2+> Ni2+. The organic calcium channel blockers ver‐apamil (20–100 μM) and nimodipine (20–50 μM) had little effect on stimulation‐induced increases in EPP amplitude. The results of this study are consistent with previous suggestions that the different components of increased release represent different mechanisms. Furthermore, if Cd2+is acting by reducing Ca2+entry into the nerve terminal, then these results suggest that facilitation and augmentation are dependent in some way on Ca2+entry. © 1993 Wiley‐Liss, Inc.