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Calcium-Activated Potassium Channels at Nodes of Ranvier Secure Axonal Spike Propagation

Type of publication Peer-reviewed
Publikationsform Original article (peer-reviewed)
Author Gründemann Jan, Gründemann Jan, Clark Beverley A.,
Project Mapping the neuronal code of fear
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Original article (peer-reviewed)

Journal Cell Reports
Volume (Issue) 12(11)
Page(s) 1715 - 1722
Title of proceedings Cell Reports
DOI 10.1016/j.celrep.2015.08.022

Abstract

© 2015 The Authors. Functional connectivity between brain regions relies on long-range signaling by myelinated axons. This is secured by saltatory action potential propagation that depends fundamentally on sodium channel availability at nodes of Ranvier. Although various potassium channel types have been anatomically localized to myelinated axons in the brain, direct evidence for their functional recruitment in maintaining node excitability is scarce. Cerebellar Purkinje cells provide continuous input to their targets in the cerebellar nuclei, reliably transmitting axonal spikes over a wide range of rates, requiring a constantly available pool of nodal sodium channels. We show that the recruitment of calcium-activated potassium channels (IK, K Ca 3.1) by local, activity-dependent calcium (Ca 2+ ) influx at nodes of Ranvier via a T-type voltage-gated Ca 2+ current provides a powerful mechanism that likely opposes depolarizing block at the nodes and is thus pivotal to securing continuous axonal spike propagation in spontaneously firing Purkinje cells. Functional connectivity between brain regions relies on long-range signaling by myelinated axons. Gründemann and Clark show that local, activity-dependent calcium influx at nodes of Ranvier recruits calcium-activated potassium channels (K Ca 3.1) that drive repolarization and sustain node excitability, providing a pivotal mechanism to secure spike propagation along Purkinje cell axons.
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