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#32735875 2020/07/28 To Up
Detailed morphological analysis of rat hippocampi treated with CSF autoantibodies from patients with anti-NMDAR encephalitis discloses two distinct types of immunostaining patterns.Anti-NMDA receptor encephalitis was first described about thirteen years ago and has become one of the most important differential diagnoses for new-onset psychosis. The disease is mediated by autoantibodies against the subunit 1 of the N-methyl-D-aspartate receptor (NMDA-R1) in patients presenting with variable clinical symptoms. Patients often profit from immunmodulatory therapy, independent of their individual symptoms. In this study CSF samples as well as monoclonal antibodies derived from patients diagnosed with NMDA-R1 encephalitis were applied to rat hippocampus and visualized by immunocytochemistry. This reveals at least two distinct patterns of immunoreactivity. Antibodies from "pattern group 1" display the familiar pattern of NMDA-R1 distribution in the hippocampus reported in experiments with rabbit anti-NMDA-R1 antibodies. Neurons and primary dendrites in the CA1 and CA3 region show strongly stained cell bodies, in line with the predominant postsynaptic localization of the NMDA receptor in the brain. However, autoantibodies from "pattern group 2" show an inverse pattern, with no staining of the cell bodies and primary dendrites in CA1 and CA3 regions. Electron microscopic experiments disclose that autoantibodies of "pattern group 1 patients" bind to postsynaptic NMDA receptors, while those of "pattern group 2 patients" target presynaptic NMDA receptors. We describe one NMDA-receptor antibody giving staining comparable to rabbit anti-NMDA-R1 antibodies, raised against the C-terminus. In the highly heterogenous disease anti-NMDA-receptor 1 encephalitis we found evidence for at least two different subtypes. It will be very interesting to determine whether there also are two distinct clinical phenotypes.
Franziska Wagner, Angelika Goertzen, Orsolya Kiraly, Gregor Laube, Jakob Kreye, Otto W Witte, Harald PrÃ¼ss, RÃ¼diger W Veh
1896 related Products with: Detailed morphological analysis of rat hippocampi treated with CSF autoantibodies from patients with anti-NMDAR encephalitis discloses two distinct types of immunostaining patterns.100ug100ug Lyophilized100ug0.1 ml100ug100ug1mg0.5 mg100ug1L100ug100ug Lyophilized
#32377661 2020/05/07 To Up
Pterostilbene prevents LPS-induced early pulmonary fibrosis by suppressing oxidative stress, inflammation and apoptosis in vivo.Early pulmonary fibrosis after acute lung injury leads to poor prognosis and high mortality. Pterostilbene (Pts), a bioactive component in blueberries, possesses anti-inflammatory, antioxidative and antifibrotic properties. However, the effects of Pts on lipopolysaccharide (LPS)-induced pulmonary fibrosis are still unknown. In our study, the Pts group showed lower lung injury and fibrosis scores, and lower levels of hydroxyproline and protein (collagen I and transforming growth factor-Î²) than the scores and levels in mice treated with LPS. MMP-1 was the degrading enzyme of collagen I and LPS caused the inhibition of MMP-1, disturbing the degradation of collagen. Additionally, Pts remarkably reversed the LPS-induced inhibition of interleukin-10 and the release of tumor necrosis factor-Î±, interleukin-6 and interleukin-1Î². In terms of cellular pathways, Pts treatment ameliorated LPS-activated nuclear factor kappa B (NF-ÎºB) and NOD-like receptor NLRP3 signaling. Besides, LPS-induced low levels of A20 could be activated by Pts. In addition, Pts treatment reversed the high levels of Caspase-3, poly ADP-ribose polymerase (PARP) and Bcl2-associated X protein (Bax) expression and the low levels of B cell lymphoma/lewkmia-2 (Bcl2) that had been induced by LPS. Moreover, oxidative stress is also involved in the pathogenesis of fibrosis. Our findings indicate that LPS injection triggered the production of myeloperoxidase (MPO) and malondialdehyde (MDA) and the depletion of superoxide dismutase (SOD) and glutathione (GSH), and that these effects were notably reversed by treatment with Pts. In addition, Pts induced the dissociation of Kelch-like epichlorohydrin-associated protein-1 (Keap-1) and NF-E2 related factor-2 (Nrf2) and the activation of downstream genes (heme oxygenase-1, NAD(P)H:quinine oxidoreductase, glutamate-cysteine ligase catalytic subunit and glutamate-cysteine ligase modifier). In conclusion, oxidative stress, apoptosis and inflammation are involved in early pulmonary fibrosis and Pts exerts a protective effect by activating Keap-1/Nrf2, inhibiting caspase-dependent A20/NF-ÎºB and NLRP3 signaling pathways.
Huahong Yang, Cong Hua, Xiaolin Yang, Xiaoye Fan, Hongyu Song, Liping Peng, Xinxin Ci
1424 related Products with: Pterostilbene prevents LPS-induced early pulmonary fibrosis by suppressing oxidative stress, inflammation and apoptosis in vivo.48 samples100 ug50 ul4 Arrays/Slide4 Sample Kit1-8 Sample Kit100ug5ug64 Membranes/Box8 Sample Kit32-50 Sample Kit
#30326345 2018/10/06 To Up
Changes in levels of cortical metabotropic glutamate 2 receptors with gender and suicide but not psychiatric diagnoses.We previously reported that, compared to controls, there are lower levels of [H]LY341495 binding to metabotropic 2/3 receptors (GRM2/3) in Brodmann's area (BA) 24, but not 17 or 46, from subjects with major depressive disorders (MDD) but not bipolar disorders (BD) or schizophrenia. To be able to better interpret these data we have now measured levels of GRM2 in two of these cortical regions.
Brian Dean, Clare Duncan, Andrew Gibbons
2185 related Products with: Changes in levels of cortical metabotropic glutamate 2 receptors with gender and suicide but not psychiatric diagnoses.25 mg100100ug Lyophilized2000 Units200ug250ul200ul200ul100
#27614006 2016/09/07 To Up
Downregulation of glutamatergic and GABAergic proteins in valproric acid associated social impairment during adolescence in mice.The etiology of Autism Spectrum Disorder (ASD) remains controversial. Deficits in social communication are one of the key criteria for ASD diagnosis. Valproic acid (VPA), which is an anti-epileptic and anti-depressive drug, is one of the teratogens to cause ASD onset. Moreover, synaptic dysfunction is suggested as one of the major causative factor in VPA-induced ASD in vitro and in vivo studies. Herein, this study aimed to determine the excitatory/inhibitory synaptic mRNA and protein expression in VPA-induced autistic mice. Pregnant BALB/c mice were injected peritoneally with a single dose of 600mg/kg VPA on embryonic day (E) 12.5. Social impairment was verified by three chamber sociability tests on postnatal days (PND) 28, 35, 42 and 49. Cortical synaptic mRNA and protein expressions were examined on PND 50. The excitatory synaptic proteins NR2A, NR2B, NR2C were significantly down-regulated by 80.0% (p<0.01), 51.5% (p<0.05) and 81.5% (p<0.05) respectively. Furthermore, the NMDAR expression regulatory protein BDNF was also found to be significantly downregulated by 76.8% (p<0.05). GAD65, GAD67, GABRA1, GABRA5, GABRB2 from the GABAergic inhibitory synaptic pathway were significantly downregulated by 21.3% (p<0.05), 77.0% (p<0.05), 53.9% (p<0.05), 56.9% (p<0.05) and 55.2% (p<0.01) respectively in the cortex of VPA-induced mice. Taken together, our results suggested that synaptic dysfunction might be involved in the social impairments in VPA-induced ASD.
Davor Kin-Fan Chau, Angus Yiu-Ting Choi, Wen Yang, Wing Nang Leung, Chun Wai Chan