Additionally, the downregulation of NR2B, p‑NR1 and p‑GluR1 in the miR‑34c agomir group demonstrated that miR‑34c may serve a negative role in cognitive function in epileptic seizures, by dysregulating NMDA and α-amino-3-hydroxy-5‑methyl‑4‑isoxazolepropionic acid receptors, which are associated with long‑term potentiation.
Our results suggest that the anti-GluN2B and anti-GluD2 antibodies may be associated with myoclonic atonic epileptic seizures and chronic cerebellitis.
Epilepsy and intellectual disability are associated with rare variants in the GluN2A and GluN2B (encoded by GRIN2A and GRIN2B) subunits of the N-methyl-D-aspartate receptor (NMDAR), a ligand-gated ion channel with essential roles in brain development and function.
In this report, we provide a detailed clinical description of a sporadic male patient with early-onset epilepsy and epileptic encephalopathy in whom we performed complete exome sequencing (WES) and identified a GRIN2B mutation.
Tonic facilitation of glutamate release by presynaptic NR2B-containing NMDA receptors is increased in the entorhinal cortex of chronically epileptic rats.
We used coimmunoprecipitation and immunoblotting techniques to quantify and compare the numbers of coassembled PSD-95 with NR2B, PSD-95 with NR1, and NR2B with NR1 in the membrane proteins of brain tissues resected from four patients (aged 3.5, 6, 14, and 18 years) with medically intractable neocortical epilepsy associated with CD.