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  HCN channel-mediated neuromodulation can control action potential velocity and fidelity in central axons

Byczkowicz, N., Eshra, A., Montanaro, J., Trevisiol, A., Hirrlinger, J., Kole, M., et al. (2019). HCN channel-mediated neuromodulation can control action potential velocity and fidelity in central axons. eLife, 8: 42766. doi:10.7554/eLife.42766.

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 Creators:
Byczkowicz, N., Author
Eshra, A., Author
Montanaro, J., Author
Trevisiol, A.1, Author           
Hirrlinger, J.1, Author           
Kole, M.H.P, Author
Shigemoto, R., Author
Hallermann, S., Author
Affiliations:
1Neurogenetics, Max Planck Institute of Experimental Medicine, Max Planck Society, ou_2173664              

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Free keywords: HCN; axon; conduction velocity; mouse; neuromodulation; neuroscience.
 Abstract: Hyperpolarization-activated cyclic-nucleotide-gated (HCN) channels control electrical
rhythmicity and excitability in the heart and brain, but the function of HCN channels at the
subcellular level in axons remains poorly understood. Here, we show that the action potential
conduction velocity in both myelinated and unmyelinated central axons can be bidirectionally
modulated by a HCN channel blocker, cyclic adenosine monophosphate (cAMP), and
neuromodulators. Recordings from mouse cerebellar mossy fiber boutons show that HCN channels
ensure reliable high-frequency firing and are strongly modulated by cAMP (EC50 40 mM; estimated
endogenous cAMP concentration 13 mM). In addition, immunogold-electron microscopy revealed
HCN2 as the dominating subunit in cerebellar mossy fibers. Computational modeling indicated that
HCN2 channels control conduction velocity primarily by altering the resting membrane potential
and are associated with significant metabolic costs. These results suggest that the cAMP-HCN
pathway provides neuromodulators with an opportunity to finely tune energy consumption and
temporal delays across axons in the brain.

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Language(s): eng - English
 Dates: 2019-09-09
 Publication Status: Published online
 Pages: 26
 Publishing info: -
 Table of Contents: -
 Rev. Type: -
 Identifiers: DOI: 10.7554/eLife.42766
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Project name : This work was supported by the German Research Foundation (DFG) (HA 6386/4–1) to SH.
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Title: eLife
Source Genre: Journal
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Pages: 26 Volume / Issue: 8 Sequence Number: 42766 Start / End Page: - Identifier: ISSN: 2050-084X