Miniature postsynaptic currents depend on Ca²⁺ released from internal stores via PLC/IP₃ pathway

Miniature postsynaptic currents (mPSCs) were examined on autaptic innervation of single rat retinal ganglion cells in low density cultures. Removal of Ca²⁺ from bath solution or blocking of Ca²⁺ channels by Cd²⁺ had no detectable effect on mPSC frequency or amplitude. Thapsigargin, an agent for mobilization of Ca²⁺ from internal stores, increased mPSC frequency 3-5-fold in control, Ca²⁺-free or Cd²⁺-containing solutions. The inositol 1,4,5-triphosphate (IP₃) receptor antagonist, heparin; the phospholipase C (PLC) inhibitor, U73122; and caffeine abolished mPSC or decreased mPSCs frequency. Calcium imaging showed that cytosolic Ca²⁺ was increased by thapsigargin and decreased by caffeine. These data demonstrate that internal store-released Ca²⁺ regulated by the PLC/IP₃/IP₃-receptor pathway has critical contribution to generation and control of miniature release in retinal ganglion cells.