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Dataset results
201 results for “Glutamate”
Ketamine Associated ACC GABA and Glutamate Change and Depression Remission:
ClinicalTrials.gov study NCT03573349. IPD Sharing: NO. Countries: 1. Publications: 3.
A Glutamate Transporter GLT1, in the Treatment of Bipolar Disorder
ClinicalTrials.gov study NCT00512616. IPD Sharing: Not stated. Countries: 1. Publications: 3.
Evenamide, a Glutamate Release Modulator, as Add-On to Standard of Care in Subjects With Documented Treatment-Resistant Schizophrenia
ClinicalTrials.gov study NCT07184619. IPD Sharing: UNDECIDED. Countries: 1. Publications: 3.
Glutamate Excitotoxicity in Brain Metastases From Lung, Breast and Melanoma Treated With Stereotactic Radiosurgery
ClinicalTrials.gov study NCT04785521. IPD Sharing: NO. Countries: 1. Publications: 7.
Effect of N-acetylcysteine on Brain Glutamate
ClinicalTrials.gov study NCT02483130. IPD Sharing: Not stated. Countries: 1. Publications: 3.
Relationship Between Efficacy of Lumateperone and Brain Glutamate and Dopamine
ClinicalTrials.gov study NCT05890768. IPD Sharing: NO. Countries: 1. Publications: 32.
Increasing Vegetable Intake Using Monosodium Glutamate: A Reduced-Effort Intervention
ClinicalTrials.gov study NCT05591612. IPD Sharing: NO. Countries: 1. Publications: 1.
Dual Anti-glutamate Therapy in Super-refractory Status Epilepticus After Cardiac Arrest
ClinicalTrials.gov study NCT05756621. IPD Sharing: UNDECIDED. Countries: 1. Publications: 10.
RNAseq data from: Medial prefrontal cortex samples of glutamate dehydrogenase-deficient mice, stress-exposed or -naive, and their Nestin-Cre+ controls
Open the record for dataset details and reuse information.
Data from: The UBR-1 ubiquitin ligase regulates glutamate metabolism to generate coordinated motor pattern in Caenorhabditis elegans
UBR1 is an E3 ubiquitin ligase best known for its ability to target protein degradation by the N-end rule. The physiological functions of UBR family proteins, however, remain not fully understood. We found that the functional loss of C. elegans UBR-1 leads to synchronized motor neuron activation, preventing body bending when animals generate reversal movements. This motor deficit is rescued by removing GOT-1, a transaminase that converts aspartate to glutamate. Both UBR-1 and GOT-1 are critically required in premotor interneurons of the reverse motor circuit to regulate the motor pattern. ubr-1 and got-1 mutants exhibit elevated and decreased glutamate level, respectively. These results raise an intriguing possibility that UBR proteins regulate glutamate metabolism.
Figure 1 from: Hristov M, Sabit Z, Kirilov T, Bakalov D, Tzoneva R, Apostolova S, Georgieva I, Andreeva-Gateva P (2024) Effects of riboflavin on hyperalgesia and serum glutamine-to-glutamate ratio in rats with painful diabetic neuropathy. Pharmacia 71: 1-7. https://doi.org/10.3897/pharmacia.71.e120921
Figure 1 Effects of riboflavin on changes in pain threshold were investigated using the paw pressure test. Streptozotocin administration significantly induced mechanical hyperalgesia by reducing the mechanical threshold and enhancing paw withdrawal responses, while supplementation with Vitamin B2 effectively mitigated mechanical hyperalgesia. Significant differences compared to the control group (Normal) are denoted as *P < 0.05, while significant differences compared to the diabetic group (Diabetic) are denoted as ##P < 0.01. n=8 animals per group.
Figure 3 from: Hristov M, Sabit Z, Kirilov T, Bakalov D, Tzoneva R, Apostolova S, Georgieva I, Andreeva-Gateva P (2024) Effects of riboflavin on hyperalgesia and serum glutamine-to-glutamate ratio in rats with painful diabetic neuropathy. Pharmacia 71: 1-7. https://doi.org/10.3897/pharmacia.71.e120921
Figure 3 Effects of riboflavin on changes in pain threshold were investigated using the formalin test. The ends of the boxes depict the 25th and 75th percentiles, with a line at the median, while error bars extend to the 10th and 90th percentiles. During phase 1 of the formalin test, neither the vehicle-treated diabetic group nor the introduction of riboflavin showed significant changes in nociceptive behavior compared to the control group. In phase 2, the vehicle-treated diabetic group exhibited increased nociceptive behavior, while the addition of 25 mg or 50 mg of vitamin B2 significantly alleviated formalin-induced hyperalgesia. Significant differences compared to the control group (Normal) are indicated as *P < 0.05. Significant differences compared to the diabetic group (Diabetic) are indicated as #P < 0.05. n=8 animals per group.
Figure 2 from: Hristov M, Sabit Z, Kirilov T, Bakalov D, Tzoneva R, Apostolova S, Georgieva I, Andreeva-Gateva P (2024) Effects of riboflavin on hyperalgesia and serum glutamine-to-glutamate ratio in rats with painful diabetic neuropathy. Pharmacia 71: 1-7. https://doi.org/10.3897/pharmacia.71.e120921
Figure 2 Effects of riboflavin on changes in pain threshold were investigated using the cold plate. Streptozotocin administration induced significant cold-induced hyperalgesia, alleviated notably by riboflavin in drinking water. Significant differences compared to the control group (Normal) are indicated as ***P < 0.001. Significant differences compared to the diabetic group (Diabetic) are indicated as #P < 0.05 and ###P < 0.001. n=8 animals per group.
Figure 4 from: Hristov M, Sabit Z, Kirilov T, Bakalov D, Tzoneva R, Apostolova S, Georgieva I, Andreeva-Gateva P (2024) Effects of riboflavin on hyperalgesia and serum glutamine-to-glutamate ratio in rats with painful diabetic neuropathy. Pharmacia 71: 1-7. https://doi.org/10.3897/pharmacia.71.e120921
Figure 4 Box plot illustrating the effect of riboflavin supplementation on the serum glutamine-to-glutamate ratio in diabetic rats. The ends of the boxes depict the 25th and 75th percentiles, with a line at the median, while error bars extend to the 10th and 90th percentiles. Riboflavin supplementation in the drinking water significantly altered the serum glutamine-to-glutamate ratio in diabetic rats with neuropathic pain, with a significant difference found only between the "Diabetic" and "Diabetic + Rf 50 mg" groups. Significant differences compared to the diabetic group (Diabetic) are indicated as *p < 0.05. n=8 animals per group.
Raw data for: Okada et al., Photopharmacological modulation of hippocampal local field potential by caged-glutamate with MicroLED probe
<p>Matlab data of LFPs (sampling rate, 1k/sec; microV)</p>
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>
Understanding Effects of Cannabis Use and Abstinence on Neural Glutamate Homeostasis
ClinicalTrials.gov study NCT05664763. IPD Sharing: NO. Countries: 1. Publications: 0.
Investigation of the Antidepressant Effects of (2R,6R)-HNK, an Enhancer of Synaptic Glutamate Release, in Treatment-Resistant Depression
ClinicalTrials.gov study NCT06511908. IPD Sharing: YES. Countries: 1. Publications: 0.
Pilot Study Effect of Sulfasalazine on Glutamate Levels by(Magnetic Resonance Spectroscopy)MRS in Patients With Glioma
ClinicalTrials.gov study NCT01577966. IPD Sharing: Not stated. Countries: 1. Publications: 0.
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Allen Brain Atlas
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Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
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