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

M H Han·A Kawasaki·J Y Wei·C J Barnstable
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Abstract

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 antago- nist, 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.

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AnimalsCaffeineCalciumCalcium ChannelsCalcium SignalingCells, CulturedEnzyme InhibitorsEstrenesExcitatory Postsynaptic PotentialsInositol 1,4,5-TrisphosphateInositol 1,4,5-Trisphosphate ReceptorsPhosphodiesterase InhibitorsPyrrolidinonesRatsRats, Long-EvansReceptors, Cytoplasmic and NuclearRetinal Ganglion CellsThapsigarginType C PhospholipasesJournal ArticleResearch Support, Non-U.S. Gov'tResearch Support, U.S. Gov't, P.H.S.

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M H Han, A Kawasaki, J Y Wei, C J Barnstable. 2001-07-20. Miniature postsynaptic currents depend on Ca2+ released from internal stores via PLC/IP3 pathway.. https://doi.org/10.1097/00001756-200107200-00032

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