Calcium influx selects the fast mode of endocytosis in the synaptic terminal of retinal bipolar cells.
To investigate the regulation of endocytosis by Ca(2+), we have made capacitance measurements in the synaptic terminal of depolarizing bipolar cells from the retina of goldfish. After a brief depolarization, all of the excess membrane was retrieved rapidly (tau approximately 1 s). But when the rise in free [Ca(2+)] was reduced by the introduction of Ca(2+) buffers [1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetate (BAPTA) or EGTA], a large fraction of the membrane was retrieved by a second, slower mechanism (tau > or = 10 s). The block of fast endocytosis by EGTA could be overcome by increasing the amplitude of the Ca(2+) current, demonstrating that Ca(2+) influx was the trigger for fast endocytosis. These manipulations of the Ca(2+) signal altered the relative proportions of fast and slow endocytosis but did not modulate the rate constants of these processes. A brief stimulus that triggered fast endocytosis did not generate a significant rise in the spatially averaged [Ca(2+)], indicating that Ca(2+) regulated endocytosis through an action close to the active zone. The slow mode of retrieval occurred at the resting [Ca(2+)]. These results demonstrate that Ca(2+) influx couples fast endocytosis and exocytosis at this synapse.
Neves
G
G
Medical Research Council Laboratory of Molecular Biology, Hills Road, Cambridge CB2 2QH, United Kingdom.
Gomis
A
A
Lagnado
L
L
D002021:Buffers; D002118:Calcium / Q000378:metabolism*; D002614:Chelating Agents; D004533:Egtazic Acid / Q000031:analogs & derivatives*; D004705:Endocytosis; D017136:Ion Transport; D008564:Membrane Potentials; D017729:Presynaptic Terminals / Q000378:metabolism* / Q000502:physiology; D012160:Retina / Q000166:cytology / Q000378:metabolism* / Q000502:physiology
D002021:Buffers; D002614:Chelating Agents; D004533:Egtazic Acid; C025603:1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid; D002118:Calcium