Endogenous calcium buffers regulate fast exocytosis in the synaptic terminal of retinal bipolar cells

Neuron. 2002 Jan 3;33(1):101-12. doi: 10.1016/s0896-6273(01)00565-7.


Calcium-triggered exocytosis at the synapse is suppressed by addition of calcium chelators, but the effects of endogenous Ca(2+) buffers have not been tested. We find that 80% of Ca(2+) binding sites in the synaptic terminal of retinal bipolar cells were associated with mobile molecules that suppressed activation of Ca(2+)-sensitive K(+) channels with an efficiency equivalent to approximately 1.2 mM BAPTA. Removing these buffers caused a 30-fold increase in the number of vesicles released by Ca(2+) tail currents lasting approximately 0.5 ms and a 2-fold increase in the rapidly releasable pool of vesicles (RRP). The effects of BAPTA and EGTA indicate that vesicles comprising the RRP were docked at variable distances from Ca(2+) channels. We propose that endogenous Ca(2+) buffers regulate the size of the RRP by suppressing the release of vesicles toward the periphery of the active zone.

MeSH terms

  • Animals
  • Calcium / metabolism*
  • Calcium Channels / drug effects
  • Calcium Channels / metabolism
  • Calcium Signaling / drug effects
  • Calcium Signaling / physiology*
  • Cells, Cultured
  • Chelating Agents / pharmacology
  • Egtazic Acid / analogs & derivatives*
  • Egtazic Acid / pharmacology
  • Electric Stimulation
  • Exocytosis / drug effects
  • Exocytosis / physiology*
  • Goldfish
  • Membrane Potentials / drug effects
  • Membrane Potentials / physiology
  • Presynaptic Terminals / drug effects
  • Presynaptic Terminals / metabolism*
  • Retina / cytology
  • Retina / drug effects
  • Retina / metabolism*
  • Synaptic Transmission / drug effects
  • Synaptic Transmission / physiology*
  • Synaptic Vesicles / drug effects
  • Synaptic Vesicles / metabolism*
  • Time Factors


  • Calcium Channels
  • Chelating Agents
  • Egtazic Acid
  • 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid
  • Calcium