NMDAR2B pSer1303 antibody Ab
- Known as:
- NMDAR2B pSer1303 (anti-) Antibody
- Catalog number:
- 1488298
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Acris antibodies
- Gene target:
- NMDAR2B pSer1303 antibody
Related genes to: NMDAR2B pSer1303 antibody Ab
- Gene:
- GRIN2B NIH gene
- Name:
- glutamate ionotropic receptor NMDA type subunit 2B
- Previous symbol:
- NMDAR2B
- Synonyms:
- GluN2B
- Chromosome:
- 12p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1992-09-18
- Date modifiied:
- 2016-02-05
Related products to: NMDAR2B pSer1303 antibody Ab
Related articles to: NMDAR2B pSer1303 antibody Ab
- Axon-carrying dendrites, AcDs, have been reported in hippocampus to be privileged dendrites which can directly feed synaptic inputs into an axonal output bypassing the soma and escaping somatic inhibition. In non-primate neocortex, 15-20% of the pyramidal cells have basal AcDs and comparable proportions occurred in organotypic cortex cultures. How does an axon happen to emerge from a dendrite? Very immature migrating pyramidal neurons have no basal dendrites but already have an axon. Sprouts were seen to emerge from the very proximal portion of axons suggesting that an AcD cell starts out as a 'dendrite-carrying axon' (DcA) cell. Further, the formation of basal AcD was influenced by neuronal activity. Inhibition of GluN2B receptors, overexpression of strongly calcium binding indicator proteins and activity deprivation impaired basal dendritic growth and reduced the proportion of AcD pyramidal neurons. In contrast, perinatal enhancement of glutamatergic network activity with kainate or carbachol via subplate neurons accelerated the appearance of AcD pyramidal neurons. None of the treatments altered the proportion of AcD interneurons. Together, the larvae stage of a cortical AcD pyramidal neuron can well be the DcA configuration, and the formation of basal AcDs was - at least transiently - regulated by neuronal activity, calcium and glutamatergic signaling. - Source: PubMed
Publication date: 2026/08/12
Bietz DavidCeylan BurakRäk AndreaKöhler InaWahle Petra - Bipolar disorder (BD) is a severe and recurrent psychiatric disorder characterized by alternating manic, hypomanic, and depressive episodes, frequent comorbidity, high relapse rates, and an increased risk of suicide. Although the pathophysiology of BD remains incompletely understood, increasing evidence suggests that DNA methylation may represent an important epigenetic regulatory layer involved in BD-related biological heterogeneity. DNA methylation alterations have been reported in genes related to dopamine, serotonin, glutamate, and gamma-aminobutyric acid (GABA) systems, suggesting a potential role in neurotransmitter dysregulation. In addition, methylation changes in genes involved in neurotrophic signaling and ion-channel function may contribute to altered neuroplasticity and neuronal excitability. Clinically, candidate methylation signatures, including brain-derived neurotrophic factor (BDNF)-related methylation changes, specific GRIN2B CpG sites, and epigenetic age acceleration (EAA), have attracted attention for their potential relevance to diagnostic differentiation, disease progression, and treatment-response research. However, these signatures have not been clinically validated, and their reproducibility, tissue specificity, and longitudinal stability remain uncertain. Mood stabilizers, including lithium, valproate, and atypical antipsychotics, may partly influence methylation-related pathways, although their epigenetic effects and clinical significance remain incompletely defined. DNA methylation-targeted interventions remain experimental and require further validation regarding specificity, safety, blood-brain barrier delivery, and clinical applicability. This review summarizes current evidence on DNA methylation abnormalities in BD, focusing on neurotransmitter systems, neuroplasticity, ion-channel excitability, circadian rhythm, immune-inflammatory regulation, candidate methylation signatures and translational challenges. We emphasize that most available findings remain associative rather than causal, and future longitudinal, brain-region-specific, cell-type-resolved, and multi-omics studies are needed to clarify the mechanistic and translational relevance of DNA methylation in BD. - Source: PubMed
Publication date: 2026/07/24
Sun LuYang YingLiu TongZhu Hang-RanWang Yi-GeHuang Ya-FeiLin Zi-XuanFeng Yan-ChenLiu Fei-Xiang - Neuropathic pain affects an estimated 7%-10% of the global population and imposes an annual economic burden exceeding $600 billion in the United States alone. It lacks robust objective biomarkers; current diagnosis relies heavily on subjective reporting and heterogeneous phenotypes. Currently utilized pain assessment tools include the brief pain inventory (BPI), numerical rating scales (0-10 pain scores), and the visual analog score (VAS), which depend on patient-reported outcomes and are influenced by social, psychological and contextual factors. This subjectivity contributes to heterogeneous phenotyping and variability (>30%) towards the treatment response. Emerging transcriptomic and epitranscriptomic evidence suggests that RNA-based biomarkers may offer a biologically sound and objective approach to understanding and managing pain by capturing underlying molecular mechanisms. Therefore, the present clinical review focused on RNA biomarker classes (mRNA, miRNA, lncRNA, RNA editing, RNA modifications) and proposes a clinically deployable testing system for diagnosis, stratification, and treatment monitoring, since there are no FDA-approved RNA-based biomarkers for pain. Therefore, this review synthesizes evidence from immune-cell transcriptomic meta-analysis (TCL1A/ERAP2), dorsal root ganglion (DRG) and central nervous system gene expression patterns (EFNB2, GABBR1, NCAM1, SCN11A)/brain genetic architecture via single-cell omics integration, and atlas-driven frameworks, like iPain single-cell atlas of pain chronification and nociceptor senescence. Additional sources include studies on RNA editing mediator adenosine deaminase acting on RNA2 (ADAR2), clinical and translational evidence supporting miRNA biomarkers, and lncRNA axes (NEAT1/miR-183-5p; H19/miR-141) as tissue-specific regulatory nodes. Additionally, m6A epitranscriptomic modifications regulated by the METTL3/METTL14 writer complex and FTO/ALKBH5 erasers, with site-specific methylation of GRIN2B mRNA shown to upregulate GluN2B in dorsal horn neurons and augment central sensitization. These biomarkers also demonstrate potential utility as pharmacodynamic readouts in drug and neuro-modulation trials. Additionally, an emerging RNA workflow technology pathway leveraging rapid low-input RNA based assays was also explained. All evidence supports the idea that these biomarkers can provide complementary insight into the mechanisms underlying pain. Although current evidence supports the feasibility of RNA-based biomarkers as indicators of key biological processes, however, the current pain biology score remains at the theoretical model stage and has not been validated through , or clinical trials. - Source: PubMed
Publication date: 2026/07/16
Soin AmolKhaira MassabSoin AvirajSoin DhilenShah ShreyasTolppi SabrinaTripathi Anubhav - N-methyl-d-aspartate (NMDA) receptors are typically composed of two NR1 subunits and two NR2 (A-D) subunits. These receptors are overactivated during excitotoxicity, which can alter the expression of their subunits. Neonatal treatment with monosodium glutamate (MSG) induces a long-lasting neurodegenerative process triggered by excitotoxicity and involving multiple alterations in neurotransmission systems. This study aimed to determine whether neonatal MSG treatment modifies the protein expression of NR1, NR2A, and NR2B subunits, and whether these changes are associated with memory impairments in adulthood. Male neonatal rats received 4 g/kg MSG subcutaneously on postnatal days (PD) 1, 3, 5, and 7. At PD 60, protein expression of NR1, NR2A, and NR2B was assessed in the cerebral motor cortex (CMC), striatum (STR), hippocampus (Hp), and entorhinal cortex (EC) using Western blot. Memory performance was evaluated between PD 55 and PD 60 using the Barnes maze and novel object recognition tests. NR1 expression did not show significant changes in any brain region analyzed. NR2A expression was significantly increased in the CMC (p< 0.001) and decreased in the STR (p< 0.01). In contrast, NR2B expression was reduced in the CMC (p< 0.05) and increased in the STR (p< 0.01) and Hp (p< 0.05). MSG-treated animals exhibited impairments in short-term spatial and working memory. These findings indicate that neonatal excitotoxicity induced by MSG leads to long-term, region-specific alterations in NMDA receptor subunit composition, which may disrupt glutamatergic signaling and contribute to cognitive deficits in adulthood. - Source: PubMed
Publication date: 2026/07/28
Castañeda-Cabral José LuisLópez-Pérez Silvia JosefinaContreras-Marín SandraCastro-Torres Rubén DaríoUreña-Guerrero Mónica Elisa - Febrile seizures (FS), the most common early-childhood neurological emergency, have a poorly understood impact on the maturing glutamatergic system. We present a detailed spatiotemporal analysis of transcriptional dynamics of key glutamatergic components during a critical postnatal window. Using a hyperthermia-induced FS model in rats at postnatal day 10, we measured mRNA levels of ionotropic (NMDA, AMPA) subunits, metabotropic glutamate receptor (mGluR) groups I-III, glutamate transporters (Slc1a1-3), and glutamine synthetase (Glul) across the dorsal/ventral hippocampus, temporal and medial prefrontal cortices at P14, P21, and P50. For selected targets (GluN2A/2B, GluA1/2, EAAT2), protein abundance was analyzed by Western blotting to test how closely transcriptional changes are reflected at the protein level. We identified robust region- and age-specific developmental trajectories for all targets, including the expected maturational shift in NMDA receptor subunits. FS disrupted these programs, causing widespread downregulation of NMDA and AMPA receptor subunits, mGluRs, and astrocytic transporters in the dorsal hippocampus and temporal cortex at P14. Importantly, FS prevented the normal developmental increase in the Grin2a/Grin2b mRNA ratio in the dorsal hippocampus at P21. Notably, protein abundance for selected targets did not mirror transcriptional changes at the examined time points, suggesting post-transcriptional buffering or delayed translation. This mismatch suggests that transcriptional changes may precede detectable proteomic alterations during circuit maturation, although alternative explanations, such as delayed translation or post-translational regulation, cannot be excluded. Our findings identify candidate transcriptional correlates that may contribute to long-term neurocognitive vulnerability, and highlight the potential importance of timing when targeting glutamatergic pathways for neuroprotection. - Source: PubMed
Publication date: 2026/07/25
Kovalenko Anna AZakharova Maria VSchwarz Alexander PZubareva Olga EZaitsev Aleksey V