Absence epilepsy and sinus dysrhythmia in mice lacking the pacemaker channel HCN2
about
Hypoosmotic cell swelling as a novel mechanism for modulation of cloned HCN2 channels.Mode shifts in the voltage gating of the mouse and human HCN2 and HCN4 channelsMolecular targets for antiepileptic drug developmentElectrical resonance with voltage-gated ion channels: perspectives from biophysical mechanisms and neural electrophysiologyModern concepts concerning the origin of the heartbeat.Cortical HCN channels: function, trafficking and plasticityEssential role of the m2R-RGS6-IKACh pathway in controlling intrinsic heart rate variabilityTwo types of interneurons in the mouse lateral geniculate nucleus are characterized by different h-current densityHomeostasis or channelopathy? Acquired cell type-specific ion channel changes in temporal lobe epilepsy and their antiepileptic potentialMechanisms of sudden unexplained death in epilepsyPacemaker activity of the human sinoatrial node: an update on the effects of mutations in HCN4 on the hyperpolarization-activated currentMolecular basis for the different activation kinetics of the pacemaker channels HCN2 and HCN4Enhanced expression of a specific hyperpolarization-activated cyclic nucleotide-gated cation channel (HCN) in surviving dentate gyrus granule cells of human and experimental epileptic hippocampusIRAG is essential for relaxation of receptor-triggered smooth muscle contraction by cGMP kinasePostnatal expression pattern of HCN channel isoforms in thalamic neurons: relationship to maturation of thalamocortical oscillations.The hyperpolarization-activated channel HCN4 is required for the generation of pacemaker action potentials in the embryonic heart.The murine HCN3 gene encodes a hyperpolarization-activated cation channel with slow kinetics and unique response to cyclic nucleotidesInhibition of cardiac pacemaker channel hHCN2 depends on intercalation of lipopolysaccharide into channel-containing membrane microdomains.Enhanced GABAA-Mediated Tonic Inhibition in Auditory Thalamus of Rats with Behavioral Evidence of Tinnitus.Mechanotransduction and hyperpolarization-activated currents contribute to spontaneous activity in mouse vestibular ganglion neuronsFunctional contributions of HCN channels in the primary auditory neurons of the mouse inner ear.HCN channels expressed in the inner ear are necessary for normal balance function.Local anesthetic inhibits hyperpolarization-activated cationic currentsSubunit-specific effects of isoflurane on neuronal Ih in HCN1 knockout mice.Suppression of ih contributes to propofol-induced inhibition of mouse cortical pyramidal neurons.Dendritic HCN channels shape excitatory postsynaptic potentials at the inner hair cell afferent synapse in the mammalian cochleaAbsence seizures in C3H/HeJ and knockout mice caused by mutation of the AMPA receptor subunit Gria4Absence epilepsy in apathetic, a spontaneous mutant mouse lacking the h channel subunit, HCN2Genetic enhancement of thalamocortical network activity by elevating alpha 1g-mediated low-voltage-activated calcium current induces pure absence epilepsy.Heterozygous mutations of the voltage-gated sodium channel SCN8A are associated with spike-wave discharges and absence epilepsy in mice.Selective participation of somatodendritic HCN channels in inhibitory but not excitatory synaptic integration in neurons of the subthalamic nucleus.Neuron-restrictive silencer factor-mediated hyperpolarization-activated cyclic nucleotide gated channelopathy in experimental temporal lobe epilepsyA molecular signature of tissues with pacemaker activity in the heart and upper urinary tract involves coexpressed hyperpolarization-activated cation and T-type Ca2+ channels.Hidden in plain sight: spike-wave discharges in mouse inbred strains.The pelvis-kidney junction contains HCN3, a hyperpolarization-activated cation channel that triggers ureter peristalsis.Distinct expression patterns of HCN channels in HL-1 cardiomyocytes.Reduction of thalamic and cortical Ih by deletion of TRIP8b produces a mouse model of human absence epilepsy.The Ih Channel Gene Promotes Synaptic Transmission and Coordinated Movement in Drosophila melanogaster.Functional characterization of a trafficking-defective HCN4 mutation, D553N, associated with cardiac arrhythmia.Cellular and network mechanisms of spike-wave seizures.
P2860
Q24538745-A4A227EE-72BD-483D-9253-A6DE3E216074Q24681855-FB0B31EF-7DB3-4FE0-BA32-380A8B9E3B33Q24683346-B0E03800-6235-4228-9F0A-CAD1A6B7DCF5Q26771354-3C5BEEDB-52F0-4E78-92E4-ECD983F77874Q27008871-8FAE8258-7918-47A8-8CE8-788E5697EAD8Q27027165-9B8B9637-E58E-48CF-B6CA-0C9E858E52EBQ27304430-BE4CA3D6-9A43-4040-BBD1-30317F66F44CQ27319461-53B8FF85-1CD2-4521-A422-2D7F28B267D0Q28080655-48434EEB-0487-4095-B221-305195255757Q28081176-0E65C2C0-A6A2-428F-8213-950BE5451F32Q28087293-0B9022B9-1288-4B78-8D4E-D617DC197E60Q28180008-80D13CC6-C378-4771-8391-CEA360BEA2BCQ28190949-DF8454F4-178D-4DDB-AB2A-646EFDD91C9BQ28513707-A14F2C03-15C7-4E11-AB87-46F8DF2EF982Q28583228-573E3186-4965-4809-A583-C298388FE29AQ28585488-8C3B2C39-1B45-4FE3-8025-B18268A774D5Q28586569-D30AD455-06E4-44B4-9AF2-56165331E274Q30317615-8A4246B5-240D-4F79-8731-874C0356807AQ30395385-12063917-58D6-4283-A01D-088893E30A78Q30410466-D5B31BB6-3994-4A22-8E41-E8AD6CDC8CDDQ30414577-AB11A3CE-07A4-4665-AAF9-4EE587739D76Q30424478-6711F40C-B1FD-4955-BE2E-8CFCFF992AF6Q30427175-D37C857E-C717-4561-996F-10285DE872E8Q30437516-C5DF6754-AB85-4AFF-BF3B-9E243B21C99EQ30437738-A1E9B6DB-8E5F-48A0-B4C1-74A89142907BQ30475679-E965D817-9280-4E7E-9E68-1032BE42A906Q30482131-F2F2C992-98B6-4DAB-8C60-99660C7C71C3Q30486037-A9AF170E-7880-4EFF-B21A-F463D03FEF2FQ30486665-2D0177B5-8E35-4602-BE8C-2D9C483C85EEQ30486948-E3F03B98-169E-4A81-BD20-A8E528F04062Q30499409-3E91C19E-B8D8-4091-BCCA-0E349C8B581CQ30504521-51F16483-7C5E-4EF3-9ED8-3420D337ECF9Q30566356-6BE01C22-5B64-46EA-AD91-1AD8E570E054Q30583453-D4189E0A-EC0C-4F20-B7DB-ED6285A27759Q30583731-38C6D307-B021-44A7-A5D6-035D429521FCQ30656532-43B4E595-9BB1-4B37-94AC-AA83CEA132E8Q30691989-87F7FD1C-F9B9-4371-9F25-F7C68436DDAEQ30839844-86DEA2A8-5314-46F1-9989-62E80581224BQ33151337-1C95B1FF-AB33-4FDB-A34B-184E66EB6652Q33227648-D8EFCA99-FE27-418E-AFBD-7E896B93D5AB
P2860
Absence epilepsy and sinus dysrhythmia in mice lacking the pacemaker channel HCN2
description
2003 nî lūn-bûn
@nan
2003年の論文
@ja
2003年学术文章
@wuu
2003年学术文章
@zh-cn
2003年学术文章
@zh-hans
2003年学术文章
@zh-my
2003年学术文章
@zh-sg
2003年學術文章
@yue
2003年學術文章
@zh
2003年學術文章
@zh-hant
name
Absence epilepsy and sinus dysrhythmia in mice lacking the pacemaker channel HCN2
@en
Absence epilepsy and sinus dysrhythmia in mice lacking the pacemaker channel HCN2.
@nl
type
label
Absence epilepsy and sinus dysrhythmia in mice lacking the pacemaker channel HCN2
@en
Absence epilepsy and sinus dysrhythmia in mice lacking the pacemaker channel HCN2.
@nl
prefLabel
Absence epilepsy and sinus dysrhythmia in mice lacking the pacemaker channel HCN2
@en
Absence epilepsy and sinus dysrhythmia in mice lacking the pacemaker channel HCN2.
@nl
P2093
P2860
P356
P1433
P1476
Absence epilepsy and sinus dysrhythmia in mice lacking the pacemaker channel HCN2
@en
P2093
Andreas Ludwig
Anke Langebartels
Carsten Wotjak
Christian Wahl
Franz Hofmann
Hans-Christian Pape
Juliane Stieber
Kenneth R Chien
Knut Holthoff
Marike Lancel
P2860
P304
P356
10.1093/EMBOJ/CDG032
P407
P577
2003-01-01T00:00:00Z