ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004
Elevated thalamic low-voltage-activated currents precede the onset of absence epilepsy in the SNAP25-deficient mouse mutant coloboma.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 82 citations in OpenAlex.
- Convergent Inhibitory Cortical Circuit Disruption Drives Genetically Distinct Absence Seizures.bioRxiv : the preprint server for biology · 2026Article
- Phenotypic diversity is caused by non-linear genetic interactions between two SNAREopathy genes.Molecular psychiatry · 2026Article
- Review
- Thalamocortical circuits in generalized epilepsy: Pathophysiologic mechanisms and therapeutic targets.Neurobiology of disease · 2023Review
- 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
- Article
- Adult loss of Cacna1a in mice recapitulates childhood absence epilepsy by distinct thalamic bursting mechanisms.Brain : a journal of neurology · 2020Article
- Genetic T-type calcium channelopathies.Journal of medical genetics · 2020Review
- Inhibition of T-Type calcium channels in mEC layer II stellate neurons reduces neuronal hyperexcitability associated with epilepsy.Epilepsy research · 2019Article
- Bad wrap: Myelin and myelin plasticity in health and disease.Developmental neurobiology · 2018Review
- The Cacna1h mutation in the GAERS model of absence epilepsy enhances T-type CaScientific reports · 2017Article
- A CaChannels (Austin, Tex.) · 2016Article
- From Molecular Circuit Dysfunction to Disease: Case Studies in Epilepsy, Traumatic Brain Injury, and Alzheimer's Disease.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 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
- SNAP-25, a Known Presynaptic Protein with Emerging Postsynaptic Functions.Frontiers in synaptic neuroscience · 2016Review
- Modulation of Cav3.2 T-type calcium channel permeability by asparagine-linked glycosylation.Channels (Austin, Tex.) · 2016Article
- Upregulation of RBFOX1 in the malformed cortex of patients with intractable epilepsy and in cultured rat neurons.International journal of molecular medicine · 2015Article
- 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
- Emerging mechanisms and consequences of calcium regulation of alternative splicing in neurons and endocrine cells.Cellular and molecular life sciences : CMLS · 2013Review
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Recessive mutations in genes encoding voltage-gated Ca2+ channel subunits alter high-voltage-activated (HVA) calcium currents, impair neurotransmitter release, and stimulate thalamic low-voltage-activated (LVA) currents that contribute to a cortical spike-wave epilepsy phenotype in mice. We now report thalamic LVA current elevations in a non-Ca2+ channel mutant. EEG analysis of Coloboma (Cm/+), an autosomal dominant mutant mouse lacking one copy of the gene for a synaptosomal-associated protein (SNAP25) that interacts with HVA channels, reveals abnormal spike-wave discharges (SWDs) in the behaving animal. We compared the biophysical properties of both LVA and HVA currents in Cm/+ and wild-type thalamic neurons and observed a 54% increase in peak current density of LVA currents evoked at -50 mV from -110 mV in Cm/+ before the developmental onset of seizures relative to control. The midpoint voltage for steady-state inactivation of LVA currents in Cm/+ was shifted in a depolarized direction by 8 mV before epilepsy onset, and the mean time constant for decay of LVA Ca2+ currents at -50 mV was also prolonged. No significant differences were found in recovery from inactivation of LVA currents or in HVA current densities and kinetics. Our data demonstrate that a non-Ca2+ channel subunit gene mutation leads to potentiated thalamic LVA currents that precede the appearance of SWDs and that altered somatodendritic HVA currents are not required for abnormal thalamocortical oscillations. We suggest that presynaptic release defects shared by these mutants lead to postsynaptic LVA excitability increases in thalamic pacemaker neurons that favor rebound bursting and absence epilepsy.
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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.