ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005
Impaired regulation of thalamic pacemaker channels through an imbalance of subunit expression in absence epilepsy.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.
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Who cites it
58 citing papers in PubMed, 1 synthesis or guideline pooled it, 112 citations in OpenAlex.
- The Contribution of HCN Channelopathies in Different Epileptic Syndromes, Mechanisms, Modulators, and Potential Treatment Targets: A Systematic Review.Frontiers in molecular neuroscience · 2022Pooled it
- Roles of funny HCN.Comparative biochemistry and physiology. Toxicology & pharmacology : CBP · 2025Review
- Hyperpolarization-activated cyclic nucleotide-gated channels and epilepsy: genetics, circuits, and treatments.Frontiers in neurology · 2025Review
- Glia instruct axon regeneration via a ternary modulation of neuronal calcium channels in Drosophila.Nature communications · 2023Article
- Thalamocortical circuits in generalized epilepsy: Pathophysiologic mechanisms and therapeutic targets.Neurobiology of disease · 2023Review
- Up-regulation of HCN2 channels in a thalamocortical circuit mediates allodynia in mice.National science review · 2023Article
- Modulation of pacemaker channel function in a model of thalamocortical hyperexcitability by demyelination and cytokines.Cerebral cortex (New York, N.Y. : 1991) · 2022Article
- Article
- The structure and function of TRIP8b, an auxiliary subunit of hyperpolarization-activated cyclic-nucleotide gated channels.Channels (Austin, Tex.) · 2020Review
- Abolishing cAMP sensitivity in HCN2 pacemaker channels induces generalized seizures.JCI insight · 2019Article
- Suppression of Hyperpolarization-Activated Cyclic Nucleotide-Gated Channel Function in Thalamocortical Neurons Prevents Genetically Determined and Pharmacologically Induced Absence Seizures.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Modulation of thalamocortical oscillations by TRIP8b, an auxiliary subunit for HCN channels.Brain structure & function · 2018Article
- Modulation of Hyperpolarization-Activated Inward Current and Thalamic Activity Modes by Different Cyclic Nucleotides.Frontiers in cellular neuroscience · 2018Article
- The Cacna1h mutation in the GAERS model of absence epilepsy enhances T-type CaScientific reports · 2017Article
- Hyperpolarization-Activated Cyclic Nucleotide-Gated (HCN) Channels in Epilepsy.Cold Spring Harbor perspectives in medicine · 2016Review
- Isolated P/Q Calcium Channel Deletion in Layer VI Corticothalamic Neurons Generates Absence Epilepsy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Disinhibition-Induced Delayed Onset of Epileptic Spike-Wave Discharges in a Five Variable Model of Cortex and Thalamus.Frontiers in computational neuroscience · 2016Article
- Involvement of HCN Channel in Muscarinic Inhibitory Action on Tonic Firing of Dorsolateral Striatal Cholinergic Interneurons.Frontiers in cellular neuroscience · 2016Article
- Reduction of thalamic and cortical Ih by deletion of TRIP8b produces a mouse model of human absence epilepsy.Neurobiology of disease · 2016Article
- The role of two-pore-domain background K⁺ (K₂p) channels in the thalamus.Pflugers Archiv : European journal of physiology · 2015Review
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of hyperpolarization-activated, cyclic nucleotide-modulated (HCN) channel isoforms and hyperpolarization-activated cation current (Ih) for seizure-related burst firing in thalamocortical (TC) neurons was investigated in a rat genetic model of absence epilepsy [Wistar Albino Glaxo rats, bred in Rijswijk (WAG/Rij)]. Burst discharges in TC neurons locked to seizure activity in vivo were prolonged during blockade of Ih by Cs+ and ZD7288 (4-ethylphenylamino-1,2-dimethyl-6-methylaminopyrimidinium chloride). In vitro analyses revealed a hyperpolarizing shift of half-maximal Ih activation (Vh) in WAG/Rij (Vh = -93.2 mV) compared with nonepileptic controls [August x Copenhagen-Irish (ACI) (Vh = -88.0 mV)]. This effect is explained by a shift of the responsiveness of Ih to cAMP toward higher concentrations in TC neurons from WAG/Rij, as revealed by application of 8-bromo-cAMP and the phosphodiesterase inhibitor IBMX. During blockade of adenylyl cyclase activity, Ih activation was similar in the two strains, whereas the difference in cAMP responsiveness persisted, thereby voting against different ambient cAMP levels between strains. Increasing the intracellular cAMP level and shifting Ih activation led to a change from burst to tonic firing mode in WAG/Rij but not in ACI rats. Furthermore, HCN1 expression was significantly increased on mRNA and protein levels, with no changes in HCN2-4 expression. In conclusion, there is an increase in HCN1 expression in the epileptic thalamus, associated with a decrease in cAMP responsiveness of Ih in TC neurons and resulting impairment to control the shift from burst to tonic firing, which, in turn, will prolong burst activity after recruitment of Ih during absence seizures.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.