ArticleProceedings of the National Academy of Sciences of the United States of America2009
Deletion of phospholipase C beta4 in thalamocortical relay nucleus leads to absence seizures.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 55 citations in OpenAlex.
- Article
- SLIT3-mediated intratumoral crosstalk induces neuroblastoma differentiation via a spontaneous regression-like program.Journal of translational medicine · 2025Article
- Phospholipase C β4 promotes RANKL-dependent osteoclastogenesis by interacting with MKK3 and p38 MAPK.Experimental & molecular medicine · 2025Article
- DNA Methylation Analysis Reveals Potential Mechanism in Takifugu rubripes Against Cryptocaryon irritans Infection.Marine biotechnology (New York, N.Y.) · 2024Article
- Thalamocortical circuits in generalized epilepsy: Pathophysiologic mechanisms and therapeutic targets.Neurobiology of disease · 2023Review
- Activation Mechanisms and Diverse Functions of Mammalian Phospholipase C.Biomolecules · 2023Review
- Cryptic mutations of PLC family members in brain disorders: recent discoveries and a deep-learning-based approach.Brain : a journal of neurology · 2023Review
- Deletion of Phospholipase C β1 in the Thalamic Reticular Nucleus Induces Absence Seizures.Experimental neurobiology · 2022Article
- The Role of Phospholipase C in GABAergic Inhibition and Its Relevance to Epilepsy.International journal of molecular sciences · 2021Review
- Clinical and experimental insight into pathophysiology, comorbidity and therapy of absence seizures.Brain : a journal of neurology · 2020Review
- Destabilization of light NREM sleep by thalamic PLCβ4 deletion impairs sleep-dependent memory consolidation.Scientific reports · 2020Article
- Adult loss of Cacna1a in mice recapitulates childhood absence epilepsy by distinct thalamic bursting mechanisms.Brain : a journal of neurology · 2020Article
- Distinct Topographical Patterns of Spike-Wave Discharge in Transgenic and Pharmacologically Induced Absence Seizure Models.Experimental neurobiology · 2019Article
- The thalamic mGluR1-PLCβ4 pathway is critical in sleep architecture.Molecular brain · 2016Article
- Hidden in plain sight: spike-wave discharges in mouse inbred strains.Genes, brain, and behavior · 2014Article
- T-type Ca2+ channels in absence epilepsy.Pflugers Archiv : European journal of physiology · 2014Review
- Acupuncture for refractory epilepsy: role of thalamus.Evidence-based complementary and alternative medicine : eCAM · 2014Review
- Sleep spindles are generated in the absence of T-type calcium channel-mediated low-threshold burst firing of thalamocortical neurons.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Understanding the basis of auriculocondylar syndrome: Insights from human, mouse and zebrafish genetic studies.American journal of medical genetics. Part C, Seminars in medical genetics · 2013Review
- CaV 2.1 ablation in cortical interneurons selectively impairs fast-spiking basket cells and causes generalized seizures.Annals of neurology · 2013Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Absence seizures are characterized by cortical spike-wave discharges (SWDs) on electroencephalography, often accompanied by a shift in the firing pattern of thalamocortical (TC) neurons from tonic to burst firing driven by T-type Ca(2+) currents. We recently demonstrated that the phospholipase C beta4 (PLCbeta4) pathway tunes the firing mode of TC neurons via the simultaneous regulation of T- and L-type Ca(2+) currents, which prompted us to investigate the contribution of TC firing modes to absence seizures. PLCbeta4-deficient TC neurons were readily shifted to the oscillatory burst firing mode after a slight hyperpolarization of membrane potential. TC-limited knockdown as well as whole-animal knockout of PLCbeta4 induced spontaneous SWDs with simultaneous behavioral arrests and increased the susceptibility to drug-induced SWDs, indicating that the deletion of thalamic PLCbeta4 leads to the genesis of absence seizures. The SWDs were effectively suppressed by thalamic infusion of a T-type, but not an L-type, Ca(2+) channel blocker. These results reveal a primary role of TC neurons in the genesis of absence seizures and provide strong evidence that an alteration of the firing property of TC neurons is sufficient to generate absence seizures. Our study presents PLCbeta4-deficient mice as a potential animal model for 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.