CALCIUM CHANNELS RESPONSIBLE FOR POTASSIUM-INDUCED TRANSMITTER RELEASE AT RAT CEREBELLAR SYNAPSES

1. The effects of calcium channel blockers on potassium-induced transmitter release were studied in thin slices of cerebellum from neonatal rats using whole-cell patch clamp methods. 2. Miniature inhibitory postsynaptic currents (mIPSCs) mediated by gamma-aminobutyric acid (GABA) were recorded from deep cerebellar nuclear neurones in the presence of tetrodotoxin. The frequency of mIPSCs was reproducibly increased by a brief application of high-potassium solution. 3. In the presence of the L-type Ca2+ channel blocker nicardipine (10 mu M), the potassium-induced increase in mIPSC frequency was suppressed by 49%. Neither the mean amplitude nor the time course of mIPSCs was affected by the blocker. 4. The N-type Ca2+ channel blocker omega-conotoxin GVIA (omega-CgTX, 3 mu M) had no effect on the frequency of potassium-induced mIPSCs. 5. The P-type Ca2+ channel blocker omega-Aga-IVA (200 nM) suppressed the potassium-induced increase in mIPSC frequency by 83% without affecting the mean amplitude or time course of mIPSCs. 6. Comparing these data with previous studies of neurally evoked transmission, it is concluded that the Ca2+ channel subtypes responsible for potassium-induced transmitter release may be different from those mediating fast synaptic transmission.