Calmodulin mediates rapid recruitment of fast-releasing synaptic vesicles at a calyx-type synapse.
In many synapses, depletion and recruitment of releasable synaptic vesicles contribute to use-dependent synaptic depression and recovery. Recently it has been shown that high-frequency presynaptic stimulation enhances recovery from depression, which may be mediated by Ca2+. We addressed this issue by measuring quantal release rates at the calyx of Held synapse and found that transmission is mediated by a heterogeneous population of vesicles, with one subset releasing rapidly and recovering slowly and another one releasing reluctantly and recovering rapidly. Ca2+ promotes refilling of the rapidly releasing synaptic vesicle pool and calmodulin inhibitors block this effect. We propose that calmodulin-dependent refilling supports recovery from synaptic depression during high-frequency trains in concert with rapid recovery of the slowly releasing vesicles.
Sakaba
T
T
Department of Membrane Biophysics, Max-Planck-Institute for Biophysical Chemistry, D-37077, Goettingen, Germany.
Neher
E
E
D000200:Action Potentials / Q000502:physiology; D000818:Animals; D001933:Brain Stem / Q000502:physiology; D002118:Calcium / Q000378:metabolism; D002147:Calmodulin / Q000378:metabolism*; D002614:Chelating Agents / Q000494:pharmacology; D004533:Egtazic Acid / Q000494:pharmacology; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D009435:Synaptic Transmission / Q000502:physiology*; D013572:Synaptic Vesicles / Q000378:metabolism*
D002147:Calmodulin; D002614:Chelating Agents; D004533:Egtazic Acid; D002118:Calcium