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Neuron. 2017 May 17;94(4):826-839.e3. doi: 10.1016/j.neuron.2017.04.020.

Synaptotagmin-7-Mediated Asynchronous Release Boosts High-Fidelity Synchronous Transmission at a Central Synapse.

Author information

1
Department of Molecular and Cellular Physiology, Stanford University, Stanford, CA 94304-5453, USA; Howard Hughes Medical Institute. Electronic address: fluo@stanford.edu.
2
Department of Molecular and Cellular Physiology, Stanford University, Stanford, CA 94304-5453, USA; Howard Hughes Medical Institute. Electronic address: tcs1@stanford.edu.

Abstract

Synchronous release triggered by Ca2+ binding to synaptotagmin-1, -2, or -9 is thought to drive fast synaptic transmission, whereas asynchronous release induced by Ca2+ binding to synaptotagmin-7 is thought to produce delayed synaptic signaling, enabling prolonged synaptic computations. However, it is unknown whether synaptotagmin-7-dependent asynchronous release performs a physiological function at fast synapses lacking a prolonged signaling mode, such as the calyx of Held synapse. Here, we show at the calyx synapse that synaptotagmin-7-dependent asynchronous release indeed does not produce a prolonged synaptic signal after a stimulus train and does not contribute to short-term plasticity, but induces a steady-state, asynchronous postsynaptic current during stimulus trains. This steady-state postsynaptic current does not increase overall synaptic transmission but instead sustains reliable generation of postsynaptic spikes that are precisely time locked to presynaptic spikes. Thus, asynchronous release surprisingly functions, at least at some synapses, to sustain high-fidelity neurotransmission driven by synchronous release during high-frequency stimulus trains.

KEYWORDS:

action potential; asynchronous release; calyx of Held; neuronal computation; neurotransmitter release; short-term plasticity; spike fidelity; synaptic transmission; synaptotagmin

PMID:
28521135
DOI:
10.1016/j.neuron.2017.04.020
[Indexed for MEDLINE]
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