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

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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.