A family of hyperpolarization-activated mammalian cation channels (original) (raw)
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- Published: 11 June 1998
Nature volume 393, pages 587–591 (1998)Cite this article
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Abstract
Pacemaker activity of spontaneously active neurons1,2,3 and heart cells4,5,6 is controlled by a depolarizing, mixed Na+/K+ current, named _I_h (or _I_f in the sinoatrial node of the heart)1,4. This current is activated on hyperpolarization of the plasma membrane. In addition to depolarizing pacemaker cells, _I_h is involved in determining the resting membrane potential of neurons1,2 and provides a mechanism to limit hyperpolarizing currents in these cells7,8,9. Hormones and neurotransmitters that induce a rise in cyclic AMP levels increase _I_h by a mechanism that is independent of protein phosphorylation, and which involves direct binding of the cyclic nucleotide to the channel that mediates _I_h10,11,12,13. Here we report the molecular cloning and functional expression of the gene encoding a hyperpolarization-activated cation channel (HAC1) that is present in brain and heart. This channel exhibits the general properties of _I_h channels. We have also identified full-length sequences of two related channels, HAC2 and HAC3, that are specifically expressed in the brain, indicating the existence of a family of hyperpolarization-activated cation channels.
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Acknowledgements
We thank P. Mayr, B. Lehnert, S. Stief and S. Ehrhard for technical support. Research was supported by grants from Deutsche Forschungsgemeinschaft and Fond der Chemischen Industrie.
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Authors and Affiliations
- Institut für Pharmakologie und Toxikologie, Technische Universität München, Biedersteiner Strasse 29, München, 80802, Germany
Andreas Ludwig, Xiangang Zong, Michael Jeglitsch, Franz Hofmann & Martin Biel
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- Andreas Ludwig
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Correspondence toMartin Biel.
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Ludwig, A., Zong, X., Jeglitsch, M. et al. A family of hyperpolarization-activated mammalian cation channels.Nature 393, 587–591 (1998). https://doi.org/10.1038/31255
- Received: 04 March 1998
- Accepted: 31 March 1998
- Issue Date: 11 June 1998
- DOI: https://doi.org/10.1038/31255