ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Enhanced NMDA receptor-dependent thalamic excitation and network oscillations in stargazer mice.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 49 citations in OpenAlex.
- Persistent input- and cell-type-specific synaptic alterations in the somatosensory thalamus of Dravet syndrome mice.Journal of neurophysiology · 2026Article
- Local thalamic interneurons drive spindle termination and enable sleep-dependent learning.bioRxiv : the preprint server for biology · 2025Article
- Investigating the Effects of NMDAR and LGI1 Antibodies on Absence Seizures: Insights from Genetic Absence Epilepsy Rats and Acute Pharmacological Model of Absence Seizures.Noro psikiyatri arsivi · 2025Article
- Microcircuit failure in STXBP1 encephalopathy leads to hyperexcitability.Cell reports. Medicine · 2023Article
- Thalamocortical circuits in generalized epilepsy: Pathophysiologic mechanisms and therapeutic targets.Neurobiology of disease · 2023Review
- Altered GABAInternational journal of molecular sciences · 2022Article
- Occurrence of hyperventilation-induced high amplitude rhythmic slowing with altered awareness after successful treatment of typical absence seizures and a network hypothesis.Clinical neurophysiology practice · 2021Article
- Hyperventilation-induced EEG slowing with altered awareness: Non-epileptic, epileptic or both?Clinical neurophysiology practice · 2021Article
- Targeting Ionotropic Glutamate Receptors in the Treatment of Epilepsy.Current neuropharmacology · 2021Review
- Clinical and experimental insight into pathophysiology, comorbidity and therapy of absence seizures.Brain : a journal of neurology · 2020Review
- Augmented Reticular Thalamic Bursting and Seizures in Scn1a-Dravet Syndrome.Cell reports · 2019Article
- Genetic rescue of absence seizures.CNS neuroscience & therapeutics · 2018Article
- Asynchronous suppression of visual cortex during absence seizures in stargazer mice.Nature communications · 2018Article
- Enhanced interlaminar excitation or reduced superficial layer inhibition in neocortex generates different spike-and-wave-like electrographic events in vitro.Journal of neurophysiology · 2018Article
- Calcineurin/NFAT Signaling in Activated Astrocytes Drives Network Hyperexcitability in Aβ-Bearing Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- NMDA Receptor Expression in the Thalamus of the Stargazer Model of Absence Epilepsy.Scientific reports · 2017Article
- Bidirectional Control of Generalized Epilepsy Networks via Rapid Real-Time Switching of Firing Mode.Neuron · 2017Article
- Synaptic Changes in AMPA Receptor Subunit Expression in Cortical Parvalbumin Interneurons in the Stargazer Model of Absence Epilepsy.Frontiers in molecular neuroscience · 2017Article
- The Edge of Stability: Response Times and Delta Oscillations in Balanced Networks.PLoS computational biology · 2016Article
- Shift in interictal relative gamma power as a novel biomarker for drug response in two mouse models of absence epilepsy.Epilepsia · 2016Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Disturbances in corticothalamic circuitry can lead to absence epilepsy. The reticular thalamic nucleus (RTN) plays a pivotal role in that it receives excitation from cortex and thalamus and, when strongly activated, can generate excessive inhibitory output and epileptic thalamocortical oscillations that depend on postinhibitory rebound. Stargazer (stg) mice have prominent absence seizures resulting from a mutant form of the AMPAR auxiliary protein stargazin. Reduced AMPAR excitation in RTN has been demonstrated previously in stg, yet the mechanisms leading from RTN hypoexcitation to epilepsy are unknown and unexpected because thalamic epileptiform oscillatory activity requires AMPARs. We demonstrate hyperexcitability in stg thalamic slices and further characterize the various excitatory inputs to RTN using electrical stimulation and laser scanning photostimulation. Patch-clamp recordings of spontaneous and evoked EPSCs in RTN neurons demonstrate reduced amplitude and increased duration of the AMPAR component with an increased amplitude NMDAR component. Short 200 Hz stimulus trains evoked a gradual approximately threefold increase in NMDAR EPSCs compared with single stimuli in wild-type (WT), indicating progressive NMDAR recruitment, whereas in stg cells, NMDAR responses were nearly maximal with single stimuli. Array tomography revealed lower synaptic, but higher perisynaptic, AMPAR density in stg RTN. Increasing NMDAR activity via reduced [Mg2+]o in WT phenocopied the thalamic hyperexcitability observed in stg, whereas changing [Mg2+]o had no effect on stg slices. These findings suggest that, in stg, a trafficking defect in synaptic AMPARs in RTN cells leads to a compensatory increase in synaptic NMDARs and enhanced thalamic excitability.
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Registered trials
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.