ArticleScientific reports2017
NMDA Receptor Expression in the Thalamus of the Stargazer Model of Absence Epilepsy.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Crocin Mitigates Glutamate Excitotoxicity and Tau Hyperphosphorylation by Modulating EAAT2 and Akt/Tau Pathway in a Scopolamine-induced Rat Model of Alzheimer's Disease.Neurochemical research · 2026Article
- Classification of Current Experimental Models of Epilepsy.Brain sciences · 2024Review
- Parvalbumin Interneuron Dysfunction in Neurological Disorders: Focus on Epilepsy and Alzheimer's Disease.International journal of molecular sciences · 2024Review
- A novel mouse model of mitochondrial disease exhibits juvenile-onset severe neurological impairment due to parvalbumin cell mitochondrial dysfunction.Communications biology · 2023Article
- Developmental Inhibitory Changes in the Primary Somatosensory Cortex of the Stargazer Mouse Model of Absence Epilepsy.Biomolecules · 2023Article
- Altered GABAInternational journal of molecular sciences · 2022Article
- The Impact of Glutamatergic Synapse Dysfunction in the Corticothalamocortical Network on Absence Seizure Generation.Frontiers in molecular neuroscience · 2022Review
- Targeting Ionotropic Glutamate Receptors in the Treatment of Epilepsy.Current neuropharmacology · 2021Review
- Dynamic Transitions of Epilepsy Waveforms Induced by Astrocyte Dysfunction and Electrical Stimulation.Neural plasticity · 2020Article
- GABABrain communications · 2020Article
- Synaptic Changes in AMPA Receptor Subunit Expression in Cortical Parvalbumin Interneurons in the Stargazer Model of Absence Epilepsy.Frontiers in molecular neuroscience · 2017Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the stargazer mouse model of absence epilepsy, altered corticothalamic excitation of reticular thalamic nucleus (RTN) neurons has been suggested to contribute to abnormal synchronicity in the corticothalamic-thalamocortical circuit, leading to spike-wave discharges, the hallmark of absence seizures. AMPA receptor expression and function are decreased in stargazer RTN, due to a mutation of AMPAR auxiliary subunit stargazin. It is unresolved and debated, however, if decreased excitation of RTN is compatible with epileptogenesis. We tested the hypothesis that relative NMDAR expression may be increased in RTN and/or thalamic synapses in stargazers using Western blot on dissected thalamic nuclei and biochemically isolated synapses, as well as immunogold cytochemistry in RTN. Expression of main NMDAR subunits was variable in stargazer RTN and relay thalamus; however, mean expression values were not statistically significantly different compared to controls. Furthermore, no systematic changes in synaptic NMDAR levels could be detected in stargazer thalamus. In contrast, AMPAR subunits were markedly decreased in both nucleus-specific and synaptic preparations. Thus, defective AMPAR trafficking in stargazer thalamus does not appear to lead to a ubiquitous compensatory increase in total and synaptic NMDAR expression, suggesting that elevated NMDAR function is not mediated by changes in protein expression in stargazer mice.
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