NDLI: Absence epilepsy and sinus dysrhythmia in mice lacking the pacemaker channel HCN2

Content Provider	PubMed Central
Author	Ludwig, Andreas Budde, Thomas Stieber, Juliane Moosmang, Sven Wahl, Christian Holthoff, Knut Anke, Langebartels Carsten, Wotjak Munsch, Thomas Zong, Xiangang Feil, Susanne Feil, Robert Lancel, Marike Chien, Kenneth R. Arthur, Konnerth Pape, Hans-christian Biel, Martin Hofmann, Franz
Copyright Year	2003
Abstract	Hyperpolarization-activated cation (HCN) channels are believed to be involved in the generation of cardiac pacemaker depolarizations as well as in the control of neuronal excitability and plasticity. The contributions of the four individual HCN channel isoforms (HCN1–4) to these diverse functions are not known. Here we show that HCN2-deficient mice exhibit spontaneous absence seizures. The thalamocortical relay neurons of these mice displayed a near complete loss of the HCN current, resulting in a pronounced hyperpolarizing shift of the resting membrane potential, an altered response to depolarizing inputs and an increased susceptibility for oscillations. HCN2-null mice also displayed cardiac sinus dysrhythmia, a reduction of the sinoatrial HCN current and a shift of the maximum diastolic potential to hyperpolarized values. Mice with cardiomyocyte- specific deletion of HCN2 displayed the same dysrhythmia as mice lacking HCN2 globally, indicating that the dysrhythmia is indeed caused by sinoatrial dysfunction. Our results define the physiological role of the HCN2 subunit as a major determinant of membrane resting potential that is required for regular cardiac and neuronal rhythmicity.
Related Links	http://dx.doi.org/10.1093/emboj/cdg032
Starting Page	216
File Format	PDF
ISSN	14602075
e-ISSN	14602075
Journal	The EMBO Journal
Issue Number	2
Volume Number	22
Language	English
Publisher	Oxford University Press
Publisher Date	2003-01-15
Access Restriction	Open
Rights Holder	Oxford University Press
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Neuroscience Immunology and Microbiology Medicine Molecular Biology

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