Mouse GRIN2A ELISA Kit
- Known as:
- Mouse GRIN2A Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- orb55999
- Product Quantity:
- 96 well
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- Mouse GRIN2A ELISA Kit
Related genes to: Mouse GRIN2A ELISA Kit
- Gene:
- GRIN2A NIH gene
- Name:
- glutamate ionotropic receptor NMDA type subunit 2A
- Previous symbol:
- NMDAR2A
- Synonyms:
- GluN2A
- Chromosome:
- 16p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1992-09-18
- Date modifiied:
- 2016-02-05
Related products to: Mouse GRIN2A ELISA Kit
Related articles to: Mouse GRIN2A ELISA Kit
- Despite being essential mediators of pain processing, the molecular identity of N-methyl-D-aspartate receptor (NMDAR) subtypes in nociceptive dorsal horn circuits is poorly understood, especially between sexes and in humans. Given the importance of GluN2 subunits in shaping NMDAR function and plasticity, we investigated the expression and localization of specific GluN2 NMDAR variants in the dorsal horn of viable spinal cord tissue from male and female rodents and human organ donors. Analysis of single-cell/nuclei sequencing datasets and quantitative reverse transcriptase polymerase chain reactions (qRT-PCR) revealed that the GluN2A () and GluN2B () subunits are robustly expressed in dorsal horn neurons of mice, rats and humans, with moderate expression of GluN2D (). Immunohistochemistry (IHC) with antigen retrieval demonstrated that GluN2A, GluN2B, and GluN2D proteins are all preferentially localized to the superficial dorsal horn of both adult rats and humans, which is conserved between males and females. Surprisingly, we found that these GluN2 NMDAR subunits are enriched in the lateral superficial dorsal horn in rats but not in humans, while presynaptic and neuronal markers are symmetrically distributed across the rat mediolateral axis. A dramatic shift in localization of GluN2A to the lateral superficial dorsal horn was observed across later postnatal development (PD21-PD90) in both male and female rats, with a corresponding change in synaptic NMDAR currents. This discovery of changes in NMDAR subunit distribution during maturation and between species will shed light on the physiological roles of NMDARs and their potential as therapeutic targets for pain. We used complementary single-cell/nuclei analysis, immunostaining, quantitative reverse transcriptase polymerase chain reactions, RNAscope in situ hybridization, and electrophysiological approaches to compare the relative expression of N-methyl-D-aspartate receptor (NMDAR) GluN2 subunits in dorsal horn spinal cord pain circuits of mouse, rat, and human spinal cord tissue. Through these comparisons, we find that the transcripts and proteins of the GluN2A, GluN2B, and GluN2D NMDAR subunits are robustly expressed in superficial dorsal horn neurons, with conserved expression across sex but important differences in expression and localization patterns across late development and between species. These discoveries shed light on the physiological roles of NMDARs and their utility as potential therapeutic targets for pain. - Source: PubMed
Publication date: 2026/05/21
Griffiths KatherineArmstrong JenniferMartin NewtonMurray-Lawson ClareOneil EstefaniaDavid Laurence STemi SantinaParnell JessicaRudyk ChristopherBursey JuliaKrajewski Jeffrey LMcDermott Jeff SDedek AnnemarieLevine Ariel JLi BaolinTsai Eve CHildebrand Michael E - Neurodegenerative diseases constitute a major public health burden, with neurotoxicity representing a critical pathogenic mechanism underlying Alzheimer's disease and Parkinson's disease. Current therapeutic approaches are primarily symptomatic and fail to prevent disease progression, highlighting the urgent need for neuroprotective agents that can modulate pathological pathways at their source. Natural fungal metabolites have emerged as promising sources of bioactive compounds with potential neuroprotective properties. This study investigates the neuroprotective potential of bioactive compounds derived from the Arctic fungus Pseudogymnoascus australis (P. australis) using an integrated in silico method. From 120 identified compounds, nine were selected based on favorable blood-brain barrier (BBB) permeability and pharmacokinetic profiles using ADMET 3.0 predictions. These included 2-aminohexadecanoic acid (AHA), 11-aminoundecanoic acid (AUA), and seven others, all exhibiting optimal drug-likeness (>0.83) and suitable CNS-targeting properties. Network pharmacology analysis identified 226 overlapping targets between the fungal compounds and neurotoxicity-associated genes. Nine hub genes (Gria1, Gria2, Gria4, Grik1, Grik2, Grin1, Grin2a, Grin2b, and Grin2c) were identified as critical nodes. Enrichment analyses revealed significant involvement in the neuroactive ligand-receptor interaction pathway, suggesting these compounds modulate ionotropic glutamate receptors. Molecular docking analysis showed strong binding affinities, with 78% of ligand-receptor complexes displaying RMSD values below 2.0 Å. AHA and Grik1 emerged as the most promising pair, with a docking score of -7.90 kcal/mol and excellent pharmacokinetic properties (drug-likeness: 0.462, BBB penetration: 0.985). Molecular dynamics simulations over 100 nanoseconds confirmed complex stability, with a mean RMSD of 2.45 Å and binding energies averaging -169.02 kcal/mol, demonstrating sustained ligand-protein interactions. These computational findings provide evidence that P. australis contains bioactive compounds capable of attenuating neurotoxicity through sustained modulation of glutamate receptors, with molecular dynamics validation supporting the thermodynamic stability and potential therapeutic relevance of these interactions. - Source: PubMed
Publication date: 2026/05/17
Naomi RuthAl-Amin MdSmykla JerzyRizman-Idid MohammedChong Teoh TeowMurthy Jaya KumarZubairi Saiful IrwanDavid PamelaSatriawan HerlandBakar Nurlizah AbuAlias Siti Aisyah - Certain events that occur in early life, such as changes in nutrition, can induce structural and functional modifications in brain development, leading to behavioral programing in the offspring. These effects depend on the timing, intensity, and duration of exposure, and may contribute to chronic disorders in adulthood. Artificial non-nutritive sweeteners (NNS), such as saccharin, have recently been proposed as potential developmental disruptors. Saccharin consumption during pregnancy is discouraged, as it can cross the placenta and accumulate in the fetus. - Source: PubMed
Publication date: 2026/04/30
Pacheco-Sánchez BeatrizLópez-Merchán RaquelRubio PabloGarcía-Martos PilarSuárez JuanSanjuan CarlosRubio LeticiaMartín-de-Las-Heras StellaRodríguez de Fonseca FernandoAlén Franciscode Ceglia MarialuisaRivera Patricia - Adolescence is associated with the emergence of several psychiatric disorders including schizophrenia. Recent studies have identified both common and rare variants of the GRIN2A gene as risk factors for schizophrenia. GRIN2A encodes the GluN2A subunit of the NMDA receptor and is developmentally regulated with low cortical expression at birth that reaches adult levels in adolescence. While global knockouts of Grin2a produce abnormal behavior in mice, little is known about the functional consequences of manipulating this gene specifically in dopamine neurons, a cell type implicated in schizophrenia pathophysiology. We find that, unlike cortical regions where GluN2A levels remain stable throughout adolescence, GluN2A naturally declines in dopamine neuron-containing brain regions in this developmental period. This suggests that adolescent dopamine neurons may be especially vulnerable to further reductions of GluN2A caused by damaging GRIN2A variants. Consistent with this idea, we find that a genetically driven reduction of Grin2a in midbrain dopamine neurons of adolescent rats is sufficient to recapitulate behaviors that are consistent with some aspects of positive symptoms of schizophrenia. These include hypersensitivity to amphetamine, diminished effort optimization, impaired ability to use feedback to modify motivated actions, and disrupted dopamine release during prediction error signaling. Computational modeling of the behavioral data further revealed reduced capacity to gate associative processes based on previous learning. These data describe a novel role for GluN2A-containing dopamine neurons in prediction error signaling and provide a rodent model to explore how mutations in GRIN2A may contribute to the latent presentation of dopamine-related symptoms in schizophrenia. - Source: PubMed
Publication date: 2026/05/13
Kielhold Michelle LJacobs David STorrado Pacheco AlejandroLefner Merridee JBogachuk Alina PLebowitz Joseph JLangdon Angela JWilliams John TZweifel Larry SMoghaddam Bita - Developmental and/or epileptic encephalopathy with spike-and-wave activation in sleep (D/EE-SWAS) represents a rare but severe group of childhood onset epilepsies characterized by sleep-potentiated epileptiform activity, seizures, and developmental stagnation or regression affecting cognition, language, and behavior. Once considered a self-limited electroencephalographic (EEG) phenomenon, D/EE-SWAS is now recognized as a disorder of brain network dysfunction in which persistent epileptiform discharges during non-rapid eye movement sleep disrupt synaptic plasticity, sleep-dependent memory consolidation, and neurodevelopmental trajectories. This review synthesizes recent advances in clinical phenotyping, genetics, neurophysiology, and therapeutics. Etiologically, D/EE-SWAS is highly heterogeneous, with pathogenic variants identified in nearly half of affected individuals, including copy number variants and single-gene disorders involving ion channels, synaptic proteins, and transcriptional regulators. GRIN2A is the most frequently implicated gene, although marked intrafamilial and interfamilial variability underscores the role of modifying genetic and network-level factors. Structural lesions-particularly those affecting thalamocortical circuits-represent another major disease substrate and are critical for treatment stratification. At the mechanistic level, abnormal thalamocortical oscillations, impaired sleep architecture, and disruption of slow-wave and spindle activity provide a pathophysiological framework linking EEG abnormalities to cognitive and behavioral deterioration. Neuroimaging and EEG-functional magnetic resonance imaging studies support a model of widespread network inhibition and disconnection extending beyond the primary epileptogenic zone. Therapeutically, corticosteroids currently represent the most effective first-line treatment, demonstrating superior cognitive outcomes compared with benzodiazepines, although relapse after tapering is common, and optimal dosing strategies remain undefined. Precision medicine approaches, including N-methyl-D-aspartate receptor-targeted therapies for GRIN variants and channel-specific treatments such as primidone for TRPM3 gain of function, offer promising avenues toward disease modification. Epilepsy surgery should be considered early in children with unilateral structural etiologies, where it can provide substantial neurodevelopmental benefit. Future priorities include standardized outcome measures, integration of sleep-based biomarkers, refinement of steroid protocols, and international collaborative trials to improve long-term neurodevelopmental outcomes in this vulnerable population. - Source: PubMed
Publication date: 2026/04/28
Specchio NicolaAuvin StéphaneBrunklaus AndreasDe Giorgis ValentinaDi Micco ValentinaGardella ElenaJansen Floor ENabbout RimaPepi ChiaraRubboli GuidoTrivisano MarinaCuratolo Paolo