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
- Since the introduction of second-generation antipsychotics, antipsychotics have been increasingly prescribed for children and adolescents, raising concerns about their long-term impact on neurodevelopment. Antipsychotics block dopaminergic and serotonergic receptors, potentially disrupting the maturation of neurocognitive processes, which is a public health concern. Previous studies have reported that adolescent antipsychotic treatment can cause persistent neurocognitive dysfunction in rodents, yet the neurobiological underpinnings remain unknown. To address this, we administered risperidone, a commonly used antipsychotic, to C57BL/6 mice during adolescence (3 to 6 weeks of age) and examined behavioral and neurobiological outcomes nine weeks post-treatment. Risperidone-treated mice exhibited subtle deficits in behavioral correlates of anxiety-like behavior. In vivo, two-photon calcium imaging of cortical neurons revealed a remarkable increase in the amplitude of calcium events with subtle sex-specific changes in the frequency, consistent with increased neuronal excitability. Single-nucleus RNA-sequencing (snRNA-seq) analyses showed widespread reductions in transcripts for voltage-sensitive and inwardly rectifying potassium channels in both pyramidal neurons and interneurons. Additionally, both cell types exhibited reduced Grin2a and Grin2b, as well as scaffolding proteins, indicative of weakened synaptic connectivity between excitatory and inhibitory neurons. Interestingly, we observed sex-dependent differences in the directionality of correlation between certain gene co-expression modules and risperidone treatment. Our results suggest that adolescent risperidone treatment induces lasting transcriptomic and functional changes associated with altered excitatory-inhibitory neuronal interactions that may underline cognitive and behavioral dysregulations. - Source: PubMed
Publication date: 2026/07/08
Alicea-Pauneto Abneil DChoi HyowonZhang WenyuLi XinjianBusque Laurence ALi MingxuanWu AndrewZhang EvanMarc Adam DPreall JonathanWang Kuan HongFeatherstone Robert ESiegel Steven JHahn Chang-GyuBorgmann-Winter Karin E - Cognitive decline is common after cancer, but little is known regarding the etiology of this adverse effect, especially in terms of molecular mechanisms. - Source: PubMed
Publication date: 2026/07/06
Kesler Shelli RFranco-Rocha Oscar YKogon ManuelaBraun SarahTolby LeahNyagaka RuthDe La Torre Schutz AlexaBlayney Douglas WPalesh Oxana - Alpha-lipoic acid (ALA) is a natural compound present in plants, animals, and humans. It provides neuroprotection through its antioxidant action, reducing oxidative stress and inflammation via pathways such as the Nrf-2 signalling pathway. It has shown protective effect against neuronal damage in Alzheimer's disease and Parkinson's disease. The traumatic brain injury (TBI) is a major cause of cognitive and motor impairments. TBI primarily initiates a series of secondary injury pathways, with glutamate excitotoxicity being a critical factor in neuronal degeneration. In this study, we investigated the protective effects of ALA on TBI induced by controlled cortical impact (CCI) in the cerebral cortex (CC) and hippocampus (HC) regions of the Wistar rats. TBI parameters were analysed using behavioural assays, including the Barnes maze test (BMT), beam balance test, grip strength, and Y-maze test (YMT). In addition, we measured brain water content, and analyzed histological alterations by light microscopy, microglial changes by the immunofluorescence technique, and ultrastructural changes by the transmission electron microscopy (TEM). Expression of markers of glutaminergic and calcium (Ca⁺) pathways was analysed by qRT-PCR and western blotting. ALA was administered following TBI induction in rats. It was shown that ALA downregulated S100B and the N-methyl-D-aspartate (NMDA) receptor subunit 2B (GRIN2B) mRNA expression. However, TBI-dependent alterations in excitatory amino acid transporter (EAAT) expression were downregulated in the CC region of adult rats with TBI. Protein expression of S100B, stromal interaction molecule (STIM), ubiquitin C-terminal hydrolase L1 (UCHL1), nuclear factor kappa (NF-ƙB), and glial fibrillary acidic protein (GFAP) was increased in the TBI group, as analysed by immunoblotting. Furthermore, expression of Iba1, a marker of microglial activation, was increased in TBI and mitigated by ALA. Overall, this study helps us understand the role of ALA as a mitigating compound in the TBI-induced rat model. - Source: PubMed
Publication date: 2026/07/01
Mazahir IqraWali BushraRehman Ahmed ShaneyDeep GauravMangla AnuradhaJindal GarimaKhan HumaParvez SuhelRaisuddin Sheikh - Clozapine is the preferred treatment for refractory schizophrenia. However, clozapine use is constrained by the risk of clozapine‑induced seizures (CISs). The molecular mechanisms behind CISs are complex and poorly understood. The objective of this study was to identify the core targets and signaling pathways contributing to CISs using network pharmacology and molecular docking. Potential targets for clozapine and seizures were screened using multiple databases, and overlapping targets were identified. Protein-protein interaction (PPI) networks were constructed using the STRING database and visualized in Cytoscape to identify core targets. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses of the core targets were performed, and a disease-target-pathway-drug network was constructed. The docking of clozapine with the core targets was evaluated to determine the stability of their interactions. Of the 656 potential targets for clozapine and 1260 targets for seizure, 104 targets overlapped. PPI analysis of the overlapping targets yielded 12 core targets. KEGG pathway enrichment analysis demonstrated that glutamatergic, dopaminergic, and GABAergic synapses may be key pathways mediating CIS. The molecular docking results showed that clozapine had strong binding affinities for the core targets, BDNF, GRIN2B, GRIN2A, and GAD1. Thus, clozapine may interfere with the glutamatergic, dopaminergic, and GABAergic synaptic pathways by modulating BDNF, GRIN2B, GRIN2A, and GAD1. Modulation of these core targets may contribute to excitatory-inhibitory imbalance in the central nervous system, thereby potentially increasing seizure susceptibility. This study provides an integrative perspective on the potential pathophysiology of CIS and suggests directions for future experimental validation and risk intervention strategies. - Source: PubMed
Publication date: 2026/06/29
Lian DaxiangLi JianHan BoLiu XiaLi RanliMa XiaoyanMao FuqiangZhuo Chuanjun - Impulse control disorders (ICDs) are a common non-motor complication in Parkinson's disease (PD) patients with multiple negative consequences for the individual and caregivers. Although ICDs are strongly linked to dopaminergic therapy, particularly dopamine agonists, only a percentage of patients develop these behaviors, suggesting the involvement of additional susceptibility factors, including genetic variability. This review aims to analyze current knowledge on the genetic background of ICDs. A literature search was conducted in the PubMed and Scopus databases for peer-reviewed research regarding the role of genetics in ICDs, published in the English language from 1996 to 2026. References of the selected articles for possible additional articles were also screened in order to include most of the key recent evidence. Genes that are involved in the dopaminergic system play a central role in ICD susceptibility, although the findings in studies are often inconsistent and not replicated. Moreover, variants in genes related to the glutamatergic (e.g., ), serotonergic (e.g., and ), and opioid systems (e.g., and ) have been implicated, supporting a multi-system contribution to ICD pathophysiology. Early recognition of genetic factors that increase susceptibility to ICDs in PD patients is awaited to increase diagnostic accuracy and expedite individualized treatment. - Source: PubMed
Publication date: 2026/05/27
Kalinderi KallirhoePapaliagkas VasileiosGoula OraioziliFidani LianaChatzidimitriou Maria