GRIA2 (phospho-Ser880) Antibody
- Known as:
- GRIA2 (phosphorilated-Ser880) Antibody
- Catalog number:
- abx000308
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- GRIA2 (phospho-Ser880) Antibody
Related genes to: GRIA2 (phospho-Ser880) Antibody
- Gene:
- GRIA2 NIH gene
- Name:
- glutamate ionotropic receptor AMPA type subunit 2
- Previous symbol:
- GLUR2
- Synonyms:
- GluA2, GLURB
- Chromosome:
- 4q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1992-02-26
- Date modifiied:
- 2016-02-05
Related products to: GRIA2 (phospho-Ser880) Antibody
Related articles to: GRIA2 (phospho-Ser880) Antibody
- Postoperative cognitive dysfunction (POCD) is a common complication of surgery in elderly patients and is characterized primarily by memory impairment; however, the underlying mechanisms remain incompletely understood. By utilizing a laparotomy model in aged mice and the delayed spatial alternation task (DSAT), we found that surgery specifically impaired the memory consolidation process. Importantly, this impairment was accompanied by significant disruption of sharp-wave ripples (SPW-R) in the hippocampal CA1 region. Previous research has indicated that trafficking of GluA2-containing AMPARs at CA3 recurrent synapses is crucial for SPW-R generation. Therefore, we examined postsynaptic AMPARs in the CA3 region after surgery and observed reduced membrane expression of GluA2-containing AMPARs, although the total protein levels and gene transcription remained unchanged. Immunofluorescence and coimmunoprecipitation revealed significantly decreased colocalization and binding of GluA2 with postsynaptic density protein 95 (PSD95), suggesting impaired synaptic GluA2 trafficking. Importantly, immediate postoperative injection of TAT-GluA2 into the CA3 region to increase GluA2 synaptic expression significantly ameliorated surgery-induced SPW-R disruption and memory consolidation deficits. Conversely, local injection of a GluA2 cross-linking agent into the CA3 region of aged mice to inhibit GluA2 trafficking mimicked the postoperative phenotypes of SPW-R disruption and memory consolidation deficits. These results reveal that surgical trauma induces impaired GluA2 trafficking at hippocampal CA3, leading to CA1 SPW-R disruption and ultimately resulting in memory consolidation deficits. This discovery provides not only a novel molecular and neural circuit explanation for the pathogenesis of POCD but also an experimental foundation for the development of neuroprotective strategies targeting GluA2 trafficking. - Source: PubMed
Publication date: 2026/07/06
Xu Zi-QingLi Xiao-WeiWang Gui-ChengWang XuWu Jiang-NanWu Ming-YuWu Ming-HuiWang Gong-MingZhang Meng-Yuan - Early-life environment may influence long-term neurodevelopment through epigenetic regulation. Serotonergic and glutamatergic pathways are central to brain development and have been implicated in DNA methylation changes following prenatal adversity. In this study, we examined whether preterm birth (PTB) in birthweight-discordant twins is associated with differential DNA methylation in the serotonin receptor signaling pathway and the glutamatergic synapse pathway in adult twins. - Source: PubMed
Publication date: 2026/06/10
Rasmussen Carl Peter VittrupNygaard MarianneNielsen Morten FrostSoerensen MetteChristensen KaareTan Qihua - Brain dysfunction is a primary symptom of Gulf War illness (GWI). The present study investigated the effects of an amorphous formula of curcumin (CUR) and α-glycosyl isoquercitrin (AGIQ) on neurobehaviors and adult neurogenesis and following synaptic plasticity of produced neurons in the hippocampal dentate gyrus (DG) in a rat GWI model. Ten-week-old rats received GWI-related chemicals and restraint stress for 28 days; thereafter, animals were fed either a diet without supplement or mixed with 0.1% CUR or 0.5% AGIQ for 126 days. GWI treatment adversely affected behavioral endpoints, including novel object recognition, sucrose preference, novelty-suppressed feeding, and contextual fear conditioning. CUR ameliorated all these effects, while AGIQ caused anxiety-like behavior and improved fear extinction learning. GWI treatment downregulated NRF2-KEAP1 pathway-related genes in the DG; both phytochemicals reversed most of these changes. GWI treatment increased CD68 and CD163 microglia populations in the DG hilus; both phytochemicals reversed the increase of CD68 microglia. In the neurogenic niche, GWI treatment decreased GFAP neural stem cells but increased DCX and PCNA cells, decreased hilar SST and GAD67 GABAergic interneurons, and downregulated Pvalb. CUR reversed decreases in GFAP cell and SST interneuron numbers. Both phytochemicals increased VGLUT1 immunoreactivity, restored the VGLUT1/VGAT ratio, and upregulated Bdnf, Gria1, Gria2, Gria3, Slc17a7, Ptgs2, and Mapk1. AGIQ further increased COX2 cell numbers and upregulated Grin2a, Grin2b, and Mapk3. In summary, both phytochemicals may have exerted antioxidant effects and modulated excitatory/inhibitory balance via glutamatergic signaling in GWI animals; CUR was superior to AGIQ at normalizing aberrant neurobehaviors and neurogenesis. - Source: PubMed
Publication date: 2026/06/25
Tang QianShobudani MomokaSakamaki YuriEbizuka YuriZou XinyuKobayashi MioKigata TetsuhitoKoyanagi MihokoNakao TomohiroShibutani Makoto - Primary liver cancer (PLC) is a leading cause of global cancer mortality. Yangzheng Xiaoji Decoction (YZXJD), a traditional Chinese medicine based on "Fuzheng Xiaoji" principles, is used as adjunctive PLC therapy, yet its underlying molecular mechanisms require further characterization. - Source: PubMed
Publication date: 2026/06/15
Yang ShengboLiu RuiWen ShuaiWang YaTai NanTian Jie - Pregabalin, a typical representative of pharmaceuticals and personal care products (PPCPs), has seen its environmental residue issue become increasingly prominent due to its widespread and high-volume clinical use. While its potential neurotoxic risks have attracted attention, the specific mechanisms underlying its induction of neurotoxicity have not yet been fully elucidated. This study investigated the neurotoxic effects of pregabalin using a zebrafish model: first, it predicted the potential mechanisms and key targets of pregabalin-induced neurotoxicity utilizing network toxicology techniques, followed by verification via experimental methods such as reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The results showed that pregabalin exposure binds to key receptors such as GRIA2, interferes with the glutamatergic synaptic pathway, thereby triggering neuronal apoptosis, and ultimately leading to neurodevelopmental impairment in zebrafish larvae - specifically a significant 8.8% reduction in neural axon length, accompanied by abnormal motor behavior, namely a significant 33.3% decrease in movement distance and a 33.4% decrease in movement speed, respectively. These findings not only provide key experimental evidence for the in-depth analysis of the neurotoxic effects and molecular mechanisms of environmental pregabalin exposure but also offer theoretical support for the systematic assessment of its eco-neurotoxic risks to ecosystems. - Source: PubMed
Publication date: 2026/06/18
Yi JunfeiLi ShumingPeng HuiLiu XuewenXi XiaotongChen Dongsheng