ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009
Genetic enhancement of thalamocortical network activity by elevating alpha 1g-mediated low-voltage-activated calcium current induces pure absence epilepsy.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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Who cites it
73 citing papers in PubMed, 141 citations in OpenAlex.
- Targeting the Complement-Microglia Axis for Neuroprotection in Pediatric Epilepsy.Biomedicines · 2026Review
- The Anticonvulsant Effect of Long-Term Valproate Might Be Attributable to Altered Expression of Selected Genes in Mice.International journal of molecular sciences · 2026Article
- Cav3.1 is a neuronal leucine sensor that mediates satiety and weight loss in response to dietary protein.Cell metabolism · 2026Article
- Genetic Animal Models of Idiopathic Generalized Epilepsies: What Can We Learn from Them?Biomedicines · 2025Review
- Molecular Mechanisms Underlying the Generation of Absence Seizures: Identification of Potential Targets for Therapeutic Intervention.International journal of molecular sciences · 2024Review
- The complex molecular epileptogenesis landscape of glioblastoma.Cell reports. Medicine · 2024Article
- A Review of theDiseases (Basel, Switzerland) · 2024Review
- Changes in the Dentate Gyrus Gene Expression Profile Induced by Levetiracetam Treatment in Rats with Mesial Temporal Lobe Epilepsy.International journal of molecular sciences · 2024Article
- Rare genetic brain disorders with overlapping neurological and psychiatric phenotypes.Nature reviews. Neurology · 2024Review
- Variant inJournal of pediatric genetics · 2023Article
- Thalamocortical circuits in generalized epilepsy: Pathophysiologic mechanisms and therapeutic targets.Neurobiology of disease · 2023Review
- Length biases in single-cell RNA sequencing of pre-mRNA.Biophysical reports · 2023Article
- MEPIRAPIM-derived synthetic cannabinoids inhibit T-type calcium channels with divergent effects on seizures in rodent models of epilepsy.Frontiers in physiology · 2023Article
- The adjustment mechanism of the spike and wave discharges in thalamic neurons: a simulation analysis.Cognitive neurodynamics · 2022Article
- Loss ofProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Novel Fluorescence-Based High-Throughput FLIPR Assay Utilizing Membrane-Tethered Genetic Calcium Sensors to Identify T-Type Calcium Channel Modulators.ACS pharmacology & translational science · 2022Article
- Small Molecules as Modulators of Voltage-Gated Calcium Channels in Neurological Disorders: State of the Art and Perspectives.Molecules (Basel, Switzerland) · 2022Review
- The Transcription Factor Shox2 Shapes Neuron Firing Properties and Suppresses Seizures by Regulation of Key Ion Channels in Thalamocortical Neurons.Cerebral cortex (New York, N.Y. : 1991) · 2021Article
- From Genotype to Phenotype: Expanding the Clinical Spectrum ofFrontiers in neurology · 2021Review
- Article
13 more citing papers are in PubMed but not listed here.
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5 authors at 2 institutions in 1 country.
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Abstract
Absence seizures are a leading form of childhood epilepsy. Human and mouse P/Q-type calcium channel gene mutations initiate a complex absence epilepsy and ataxia phenotype, and in mice, secondarily elevate neuronal low-voltage-activated T-type calcium currents. These currents influence thalamocortical network activity and contribute to the generation of cortical spike-wave discharges (SWDs) associated with absence seizures. To address whether enhanced thalamocortical T-type currents suffice to induce an epileptic phenotype, two BAC transgenic mouse lines overexpressing the Cacna1g gene for alpha1G T-type calcium channels were generated with low and high transgene copy numbers that exhibit elevated alpha1G expression and showed increased functional T-type currents measured in thalamic neurons. Both lines exhibit frequent bilateral cortical SWDs associated with behavioral arrest but lack other overt neurological abnormalities. These models provide the first evidence that primary elevation of brain T-type currents are causally related to pure absence epilepsy, and selectively identify Cacna1g, one of the three T-type calcium channel genes, as a key component of a genetically complex epileptogenic pathway.
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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.