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29 results for “glutamate receptors”
Image quantification data for: Activity-dependent mitochondrial ROS signaling regulates recruitment of glutamate receptors to synapses
<p>Our understanding of mitochondrial signaling in the nervous system has been limited by the technical challenge of analyzing mitochondrial function <em>in vivo</em>. In the transparent genetic model <em>Caenorhabditis elegans, </em>we were able to manipulate and measure mitochondrial ROS (reactive oxygen species) signaling of individual mitochondria as well as neuronal activity of single neurons <em>in vivo</em>. Using this approach, we provide evidence supporting a novel role for mitochondrial ROS signaling in dendrites of excitatory glutamatergic <em>C. elegans</em> interneurons. Specifically, we show that following neuronal activity, dendritic mitochondria take up calcium (Ca<sup>2+</sup>) via the mitochondrial Ca<sup>2+</sup> uniporter MCU-1 which results in an upregulation of mitochondrial ROS production. We also observed that mitochondria are positioned in close proximity to synaptic clusters of GLR-1, the <em>C. elegans</em> ortholog of the AMPA subtype of glutamate receptors that mediate neuronal excitation. We show that synaptic recruitment of GLR-1 is upregulated when MCU-1 function is pharmacologically or genetically impaired but is downregulated by mitoROS signaling. Thus, signaling from postsynaptic mitochondria may regulate excitatory synapse function to maintain neuronal homeostasis by preventing excitotoxicity and energy depletion.</p>
Activity-dependent mitochondrial ROS signaling regulates recruitment of glutamate receptors to synapses
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Evidence for the association between the intronic haplotypes of ionotropic glutamate receptors and schizophrenia
<p>VCF and BED files for the publication "Evidence for the association between the intronic haplotypes of ionotropic glutamate receptors and schizophrenia".</p>
Brain Glutamate Receptors and Cocaine Dependence
ClinicalTrials.gov study NCT00951314. IPD Sharing: Not stated. Countries: 1. Publications: 3.
Data from: Glutamate receptor delta2 serum antibodies in paediatric opsoclonus myoclonus ataxia syndrome
Objective: To identify neuronal surface antibodies in opsoclonus myoclonus ataxia syndrome (OMAS) usingcontemporary antigen discovery methodology. Methods: OMAS patient serum IgG immunohistochemistry using age-equivalent rat cerebellar tissue was followed by immunoprecipitation, gel electrophoresis and mass spectrometry. Data are available via ProteomeXchange (identifier PXD009578). This generated a list of potential neuronal surface cerebellar autoantigens. Live cell-based assays (CBA) were used to confirm membrane-surface antigens and adsorb antigen-specific IgGs. The serological results were compared to the clinical data. Results: Four of the six OMAS sera tested bound rat cerebellar sections. Two of these sera with similar immunoreactivities were used in immunoprecipitation experiments using cerebellum from postnatal rat pups (P18). Mass spectrometry identified 12 cell-surface proteins, of which glutamate receptor delta 2 (GluD2), a predominately cerebellar-expressed protein, was found at a threefold higher concentration than the other 11 proteins. Antibodies to GluD2 were identified in 14/16 (87%) OMAS samples, compared with 5/139 (5%) pediatric and 1/38 (2.6%) adult serum controls (p<0.0001), and in 2/4 sera from patients with neuroblastoma without neurological features. Adsorption of positive OMAS sera against GluD2-transfected cells substantially reduced but did not eliminate, reactivity towards cerebellar sections. Conclusion: Autoantibodies to GluD2 are frequent in patients with OMAS, bind to surface determinants and are potentially pathogenic.
Targeting metabotropic glutamate receptor 4 for cancer immunotherapy
<p><span><span><span><span><span><span><span><span><span><span><span>The complex mechanism regulating the immunosuppressive tumor microenvironment (TME) remains poorly understood. Here, we reported a novel role of the metabotropic glutamate receptor-4 (GRM4) in suppressing the anti-tumor immunity. We revealed in three murine syngeneic tumor models (B16, MC38, and 3LL) that either genetic knockout (<i>Grm4</i><sup>−/−</sup>) or pharmacological inhibition led to significant delay in tumor growth and synergized with immune checkpoint inhibitors in male mice. Mechanistically, perturbation of GRM4 resulted in a strong anti-tumor immunity by promoting nature killer (NK), CD4<sup>+</sup> and CD8<sup>+</sup> T cells towards an activated, proliferative, and functional phenotype. Single-cell RNA-sequencing and T Cell Receptor (TCR) profiling further defined the clonal expansion and immune landscape changes in CD8<sup>+</sup> T cells. Mechanistically, <i>Grm4</i><sup>-/- </sup>intrinsically activated IFN-g production in CD8<sup>+</sup> T cells through cAMP/CREB-mediated pathway. Our study appears to be of clinical significance as a signature of NK<sup>high</sup>-GRM4<sup>low</sup> and CD8<sup>high</sup>-GRM4<sup>low</sup> correlated with improved survival in melanoma patients. Therefore, targeting GRM4 could be exploited as a new approach for cancer immunotherapy. </span></span></span></span></span></span></span></span></span></span></span></p>
Data from: Molecular dynamics investigation of gluazo, a photo-switchable ligand for the glutamate receptor GluK2
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Data from: Glutamate receptor delta2 serum antibodies in paediatric opsoclonus myoclonus ataxia syndrome
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Targeting metabotropic glutamate receptor 4 for cancer immunotherapy
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Identification and therapeutic rescue of autophagosome and glutamate receptor defects in C9ORF72 and sporadic ALS neurons
GEO Series GSE133162. Homo sapiens. 4 samples. Type: Expression profiling by high throughput sequencing.
The Estrogen Receptor Co-Regulator Protein, Proline Glutamic Acid and Leucine Rich Protein 1 (PELP1) Mediates Estrogen Rapid Signaling and Neuroprotection in the Brain
GEO Series GSE72136. Mus musculus. 4 samples. Type: Expression profiling by high throughput sequencing.
Targeting postsynaptic glutamate receptor scaffolding proteins PSD-95 and PICK1 for obesity treatment
GEO Series GSE221549. Mus musculus. 47 samples. Type: Expression profiling by high throughput sequencing.
Targeting postsynaptic glutamate receptor scaffolding proteins PSD-95 and PICK1 for obesity treatment [2]
GEO Series GSE251836. Mus musculus. 24 samples. Type: Expression profiling by high throughput sequencing.
Data from: Molecular determinants of agonist selectivity in glutamate-gated chloride channels which likely explain the agonist selectivity of the vertebrate glycine and GABAA-ρ receptors
Orthologous Cys-loop glutamate-gated chloride channels (GluClR's) have been cloned and described electrophysiologically and pharmacologically in arthropods and nematodes (both members of the invertebrate ecdysozoan superphylum). Recently, GluClR's from Aplysia californica (a mollusc from the lophotrochozoan superphylum) have been cloned and similarly studied. In spite of sharing a common function, the ecdysozoan and lophotrochozoan receptors have been shown by phylogenetic analyses to have evolved independently. The recent crystallization of the GluClR from C. elegans revealed the binding pocket of the nematode receptor. An alignment of the protein sequences of the nematode and molluscan GluClRs showed that the Aplysia receptor does not contain all of the residues defining the binding mode of the ecdysozoan receptor. That the two receptors have slightly different binding modes is not surprising since earlier electrophysiological and pharmacological experiments had suggested that they were differentially responsive to certain agonists. Knowledge of the structure of the C. elegans GluClR has permitted us to generate a homology model of the binding pocket of the Aplysia receptor. We have analyzed the differences between the two binding modes and evaluated the relative significance of their non-common residues. We have compared the GluClRs electrophysiologically and pharmacologically and we have used site-directed mutagenesis on both receptor types to test predictions made from the model. Finally, we propose an explanation derived from the model for why the nematode receptors are gated only by glutamate, whereas the molluscan receptors can also be activated by β-alanine, GABA and taurine. Like the Aplysia receptor, the vertebrate glycine and GABAA-ρ receptors also respond to these other agonists. An alignment of the sequences of the molluscan and vertebrate receptors shows that the reasons we have given for the ability of the other agonists to activate the Aplysia receptor also explain the agonist profile seen in the glycine and GABAA-ρ receptors.
Role of Antibodies Against Glutamate Receptors and Double Stranded DNA in Epilepsy Patients
ClinicalTrials.gov study NCT00317668. IPD Sharing: Not stated. Countries: 1. Publications: 0.
Does Subacromial Injection With Glutamate Receptor Antagonist, Ketamine, Attenuate Pain in Rotator Cuff Tendinopathy?
ClinicalTrials.gov study NCT02967640. IPD Sharing: NO. Countries: 1. Publications: 0.
The Expression of the Ionotropic Glutamate Receptors in Colon of IBS
ClinicalTrials.gov study NCT02512146. IPD Sharing: Not stated. Countries: 1. Publications: 0.
Metabotropic Glutamate Receptor-5 (mGlur5) Effects on Reward-Related fMRI-BOLD Activation in FHP and FHN
ClinicalTrials.gov study NCT03341715. IPD Sharing: Not stated. Countries: 1. Publications: 0.
Development of a Novel Glutamate Receptor Ligand for PET Scans in Neuropsychiatric Systemic Lupus Erythematosus
ClinicalTrials.gov study NCT02456168. IPD Sharing: Not stated. Countries: 1. Publications: 0.
Data from: Molecular determinants of agonist selectivity in glutamate-gated chloride channels which likely explain the agonist selectivity of the vertebrate glycine and GABAA-ρ receptors
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