Coupling of L type calcium channels with ryanodine receptors in presynaptic nerve terminals

采用全细胞膜片钳技术研究了在细胞外无Ca^<2+>条件下，钾诱导的突触前去极化对自发突触后电流的影响。士的宁完全抑制了自发突触电流，表明它们是甘氨酸能抑制性突触后电流（IPSCs）。即使在没有细胞外Ca^<2+>的情况下，细胞外K^+浓度的升高也可逆地增加了自发IPSCs的频率。河豚毒素对钾诱导的突触增强无影响。在没有细胞外Na^+的情况下，钾诱导的IPSC频率增加也被观察到。然而，在无Na^+的条件下，突触增强的恢复明显受到抑制。通过thapsigargin消耗细胞内Ca^<2+>储存，可以阻止钾诱导的自发IPSCs的促进，这表明Ca^<2+>-释放来自细胞内Ca^<2+>储存。这些结果揭示了钾诱导的去极化调节突触前神经末梢细胞内Ca^<2+>浓度和胞外分泌的新机制。

The effect of potassium-induced presynaptic depolarization on spontaneous postsynaptic currents under extracellular Ca^<2+>-free conditions was investigated in mechanically dissociated rat spinal cord neurons using whole-cell patch-clamp technique. Spontaneous synaptic currents were fully inhibited by application of strychnine, indicating that they were glycinergic inhibitory postsynaptic currents (IPSCs). Elevating extracellular K^+ concentration reversibly increased that frequency of spontaneous IPSCs even in the absence of extracellular Ca^<2+>. Tetrodotoxin had no effect on the potassium-induced synaptic potentiation. The potassium-induced increase in IPSC frequency was also observed in the absence of extracellular Na^+. However, the recovery from the synaptic potentiation was markedly inhibited in the Na^+-free conditions. The potassium-induced facilitation of spontaneous IPSCs was prevented by depletion of intracellular Ca^<2+> store with thapsigargin, suggesting the contribution of Ca^<2+>-release from intracellular Ca^<2+> stores.These results reveal a novel mechanism by which potassium-induced depolarization regulates the intracellular Ca^<2+> concentration and exocytosis in presynaptic nerve terminals.