KCNQ5 channels control resting properties and release probability of a synapse

Research output: Contribution to journalArticle

42 Citations (Scopus)

Abstract

Little is known about which ion channels determine the resting electrical properties of presynaptic membranes. In recordings made from the rat calyx of Held, a giant mammalian terminal, we found resting potential to be controlled by KCNQ (Kv7) K+ channels, most probably KCNQ5 (Kv7.5) homomers. Unlike most KCNQ channels, which are activated only by depolarizing stimuli, the presynaptic channels began to activate just below the resting potential. As a result, blockers and activators of KCNQ5 depolarized or hyperpolarized nerve terminals, respectively, markedly altering resting conductance. Moreover, the background conductance set by KCNQ5 channels, together with Na+ and hyperpolarization-activated and cyclic nucleotide-gated (HCN) channels, determined the size and time course of the response to subthreshold stimuli. Signaling pathways known to directly affect exocytic machinery also regulated KCNQ5 channels, and increase or decrease of KCNQ5 channel activity controlled release probability through alterations in resting potential. Thus, ion channel determinants of presynaptic resting potential also control synaptic strength.

Original languageEnglish (US)
Pages (from-to)840-847
Number of pages8
JournalNature Neuroscience
Volume14
Issue number7
DOIs
StatePublished - Jul 2011

Fingerprint

Membrane Potentials
Synapses
Ion Channels
Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels
Membranes

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

KCNQ5 channels control resting properties and release probability of a synapse. / Huang, Hai; Trussell, Laurence.

In: Nature Neuroscience, Vol. 14, No. 7, 07.2011, p. 840-847.

Research output: Contribution to journalArticle

@article{d7f9849a215b4a27aa00ca289b49202c,
title = "KCNQ5 channels control resting properties and release probability of a synapse",
abstract = "Little is known about which ion channels determine the resting electrical properties of presynaptic membranes. In recordings made from the rat calyx of Held, a giant mammalian terminal, we found resting potential to be controlled by KCNQ (Kv7) K+ channels, most probably KCNQ5 (Kv7.5) homomers. Unlike most KCNQ channels, which are activated only by depolarizing stimuli, the presynaptic channels began to activate just below the resting potential. As a result, blockers and activators of KCNQ5 depolarized or hyperpolarized nerve terminals, respectively, markedly altering resting conductance. Moreover, the background conductance set by KCNQ5 channels, together with Na+ and hyperpolarization-activated and cyclic nucleotide-gated (HCN) channels, determined the size and time course of the response to subthreshold stimuli. Signaling pathways known to directly affect exocytic machinery also regulated KCNQ5 channels, and increase or decrease of KCNQ5 channel activity controlled release probability through alterations in resting potential. Thus, ion channel determinants of presynaptic resting potential also control synaptic strength.",
author = "Hai Huang and Laurence Trussell",
year = "2011",
month = "7",
doi = "10.1038/nn.2830",
language = "English (US)",
volume = "14",
pages = "840--847",
journal = "Nature Neuroscience",
issn = "1097-6256",
publisher = "Nature Publishing Group",
number = "7",

}

TY - JOUR

T1 - KCNQ5 channels control resting properties and release probability of a synapse

AU - Huang, Hai

AU - Trussell, Laurence

PY - 2011/7

Y1 - 2011/7

N2 - Little is known about which ion channels determine the resting electrical properties of presynaptic membranes. In recordings made from the rat calyx of Held, a giant mammalian terminal, we found resting potential to be controlled by KCNQ (Kv7) K+ channels, most probably KCNQ5 (Kv7.5) homomers. Unlike most KCNQ channels, which are activated only by depolarizing stimuli, the presynaptic channels began to activate just below the resting potential. As a result, blockers and activators of KCNQ5 depolarized or hyperpolarized nerve terminals, respectively, markedly altering resting conductance. Moreover, the background conductance set by KCNQ5 channels, together with Na+ and hyperpolarization-activated and cyclic nucleotide-gated (HCN) channels, determined the size and time course of the response to subthreshold stimuli. Signaling pathways known to directly affect exocytic machinery also regulated KCNQ5 channels, and increase or decrease of KCNQ5 channel activity controlled release probability through alterations in resting potential. Thus, ion channel determinants of presynaptic resting potential also control synaptic strength.

AB - Little is known about which ion channels determine the resting electrical properties of presynaptic membranes. In recordings made from the rat calyx of Held, a giant mammalian terminal, we found resting potential to be controlled by KCNQ (Kv7) K+ channels, most probably KCNQ5 (Kv7.5) homomers. Unlike most KCNQ channels, which are activated only by depolarizing stimuli, the presynaptic channels began to activate just below the resting potential. As a result, blockers and activators of KCNQ5 depolarized or hyperpolarized nerve terminals, respectively, markedly altering resting conductance. Moreover, the background conductance set by KCNQ5 channels, together with Na+ and hyperpolarization-activated and cyclic nucleotide-gated (HCN) channels, determined the size and time course of the response to subthreshold stimuli. Signaling pathways known to directly affect exocytic machinery also regulated KCNQ5 channels, and increase or decrease of KCNQ5 channel activity controlled release probability through alterations in resting potential. Thus, ion channel determinants of presynaptic resting potential also control synaptic strength.

UR - http://www.scopus.com/inward/record.url?scp=79959660840&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=79959660840&partnerID=8YFLogxK

U2 - 10.1038/nn.2830

DO - 10.1038/nn.2830

M3 - Article

VL - 14

SP - 840

EP - 847

JO - Nature Neuroscience

JF - Nature Neuroscience

SN - 1097-6256

IS - 7

ER -