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Enhancing the fidelity of neurotransmission by activity-dependent facilitation of presynaptic potassium currents.


ABSTRACT: Neurons convey information in bursts of spikes across chemical synapses where the fidelity of information transfer critically depends on synaptic input-output relationship. With a limited number of synaptic vesicles (SVs) in the readily releasable pool (RRP), how nerve terminals sustain transmitter release during intense activity remains poorly understood. Here we report that presynaptic K(+) currents evoked by spikes facilitate in a Ca(2+)-independent but frequency- and voltage-dependent manner. Experimental evidence and computer simulations demonstrate that this facilitation originates from dynamic transition of intermediate gating states of voltage-gated K(+) channels (Kvs), and specifically attenuates spike amplitude and inter-spike potential during high-frequency firing. Single or paired recordings from a mammalian central synapse further reveal that facilitation of Kvs constrains presynaptic Ca(2+) influx, thereby efficiently allocating SVs in the RRP to drive postsynaptic spiking at high rates. We conclude that presynaptic Kv facilitation imparts neurons with a powerful control of transmitter release to dynamically support high-fidelity neurotransmission.

SUBMITTER: Yang YM 

PROVIDER: S-EPMC4503407 | biostudies-literature | 2014 Jul

REPOSITORIES: biostudies-literature

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Enhancing the fidelity of neurotransmission by activity-dependent facilitation of presynaptic potassium currents.

Yang Yi-Mei YM   Wang Wei W   Fedchyshyn Michael J MJ   Zhou Zhuan Z   Ding Jiuping J   Wang Lu-Yang LY  

Nature communications 20140731


Neurons convey information in bursts of spikes across chemical synapses where the fidelity of information transfer critically depends on synaptic input-output relationship. With a limited number of synaptic vesicles (SVs) in the readily releasable pool (RRP), how nerve terminals sustain transmitter release during intense activity remains poorly understood. Here we report that presynaptic K(+) currents evoked by spikes facilitate in a Ca(2+)-independent but frequency- and voltage-dependent manner  ...[more]

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