ArticleJournal of neurophysiology2022
GluN3 subunit expression correlates with increased vulnerability of hippocampus and entorhinal cortex to neurodegeneration in a model of temporal lobe epilepsy.
Article in Journal of neurophysiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- Chronic Alcohol Exposure Alters Expression of GluN3A-NMDA Receptors in Adult VTA DA Neurons.bioRxiv : the preprint server for biology · 2026Article
- Aberrant histone acetylation and dysregulated synaptic plasticity in cognitive impairment induced by a high-methionine diet.Neural regeneration research · 2026Article
- Discrete interneuron subsets participate in GluN1/GluN3A excitatory glycine receptor (eGlyR)-mediated regulation of hippocampal network activity throughout development and evolution.Research square · 2025Article
- Discrete interneuron subsets participate in GluN1/GluN3A excitatory glycine receptor (eGlyR)-mediated regulation of hippocampal network activity throughout development and evolution.bioRxiv : the preprint server for biology · 2025Article
- The DEC2-SCN2A Axis is Essential for the Anticonvulsant Effects of Cannabidiol by Modulating Neuronal Plasticity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Visualizing the triheteromeric N-methyl-D-aspartate receptor subunit composition.Frontiers in synaptic neuroscience · 2023Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Temporal lobe epilepsy (TLE) is the most common type of epilepsy in adults that is often refractory to antiepileptic medication therapy. Neither the pathology nor the etiology of TLE is fully characterized, although recent studies have established that the two are causally related. TLE pathology entails a stereotypic pattern of neuron loss in hippocampal and parahippocampal regions, predominantly in CA1 subfield of the hippocampus and layer 3 of the medial entorhinal area (MEA), deemed hallmark pathological features of the disease. Through this work, we address the contribution of glutamatergic
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Registered trials
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