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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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Byczkowicz+19_Elife_.pdf (Publisher version), 4MB
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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
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 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