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201 results for “Glutamate”
Dataset for the publication: Electrochemical transformation of D,L-glutamic acid into acrylonitrile
<p>The dataset comprehends the experimental data used as basis of the contribution on the electrochemical transformation of D,L-glutamic acid into acrylonitrile. The electrochemical transformation of D,L‑glutamic acid as substrate proceeds in several steps via electro-oxidative decarboxylation and non-Kolbe electrolysis. The provided data comprehend yields and faradaic efficiencies of the transformations under different reaction conditions.</p>
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>
Supporting files for Turečková et al. 2024 "A New Abscisic Acid Conjugate, ABA‑L‑Glutamate, Determined in Different Plant Species by Combined Immunoaffinity Chromatography‑Tandem Mass Spectrometry"
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Astrocytic Gi-GPCR activation enhances stimulus-evoked extracellular glutamate
<p>Astrocytes perform critical functions in the nervous system, many of which are dependent on neurotransmitter-sensing through G protein-coupled receptors (GPCRs). However, whether specific astrocytic outputs follow specific GPCR activity remains unclear, and exploring this question is critical for understanding how astrocytes ultimately influence brain function and behavior. Here, we investigate the outputs of astrocytic Gi-GPCRs, a family of GPCRs which we previously showed is sufficient to increase slow-wave neural activity (SWA) during sleep when activated in cortical astrocytes<sup>1</sup>. We focus on two putative outputs by astrocytes <em>in vivo</em>, the regulation of extracellular glutamate and GABA, by combining fiber photometry recordings of the extracellular indicators iGluSnFR and iGABASnFR with astrocyte-specific chemogenetic Gi-GPCR activation. We find that Gi-GPCR activation does not change spontaneous dynamics of extracellular glutamate or GABA. However, Gi-GPCR activation does specifically increase visual stimulus-evoked extracellular glutamate. Together, these data point towards a complex relationship between astrocytic inputs and outputs <em>in vivo </em>that may depend on behavioral context. Further, they suggest an extracellular glutamate-specific mechanism underlying some astrocytic Gi-GPCR-dependent behaviors, including the regulation of sleep SWA.</p>
Activity-dependent mitochondrial ROS signaling regulates recruitment of glutamate receptors to synapses
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Astrocytic Gi-GPCR activation enhances stimulus-evoked extracellular glutamate
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Data from: Effects of fluorescent glutamate indicators on neurotransmitter diffusion and uptake
Genetically encoded fluorescent glutamate indicators (iGluSnFRs) enable neurotransmitter release and diffusion to be visualized in intact tissue. Synaptic iGluSnFR signal time courses vary widely depending on experimental conditions, often lasting 10-100 times longer than the extracellular lifetime of synaptically released glutamate estimated with uptake measurements. iGluSnFR signals typically also decay much more slowly than the unbinding kinetics of the indicator. To resolve these discrepancies, here we have modeled synaptic glutamate diffusion, uptake and iGluSnFR activation to identify factors influencing iGluSnFR signal waveforms. Simulations suggested that iGluSnFR competes with transporters to bind synaptically released glutamate, delaying glutamate uptake. Accordingly, synaptic transporter currents recorded from iGluSnFR-expressing astrocytes in mouse cortex were slower than those in control astrocytes. Simulations also suggested that iGluSnFR reduces free glutamate levels in extrasynaptic spaces, likely limiting extrasynaptic receptor activation. iGluSnFR and lower-affinity variants nonetheless provide linear indications of vesicle release, underscoring their value for optical quantal analysis.
3D localization AFM (3D-LAFM) density map of glutamate transporter GltPh outward facing state (OFS) conformation at apo condition, imaged from the cytoplasmic side
<p>3D localization AFM (3D-LAFM) density map of glutamate transporter GltPh outward facing state (OFS) conformation at apo condition, imaged from the cytoplasmic side, in <code>.afm</code> format and in <code>.mrc</code> format.</p> <p>Note: The <code>.afm</code> file encodes details for constructing 3D-LAFM density maps and includes experimental conditions in its header. Using <code>.afm</code> files requires the additional installation of the AFM file encoder (available from <a href="https://github.com/rafaeljiang23/3D-LAFM/tree/main/ChimeraX-AfmFormat_v2">GitHub</a>). Once the relevant installation is complete, <code>.afm</code> files can be opened in ChimeraX via drag-and-drop. In contrast, <code>.mrc</code> files, which encode only the density values equivalent to <code>.afm</code> files, can be directly opened in ChimeraX without requiring additional software installation.</p> <p>The deposited <code>.afm</code> file follows the 'AFM1' (metacode) format standard.</p>
3D localization AFM (3D-LAFM) density map of glutamate transporter GltPh inward facing state closed (IFSclosed) conformation at apo condition, imaged from the cytoplasmic side
<p>3D localization AFM (3D-LAFM) density map of glutamate transporter GltPh inward facing state closed (IFSclosed) conformation at apo condition, imaged from the cytoplasmic side, in <code>.afm</code> format and in <code>.mrc</code> format.</p> <p>Note: The <code>.afm</code> file encodes details for constructing 3D-LAFM density maps and includes experimental conditions in its header. Using <code>.afm</code> files requires the additional installation of the AFM file encoder (available from <a href="https://github.com/rafaeljiang23/3D-LAFM/tree/main/ChimeraX-AfmFormat_v2">GitHub</a>). Once the relevant installation is complete, <code>.afm</code> files can be opened in ChimeraX via drag-and-drop. In contrast, <code>.mrc</code> files, which encode only the density values equivalent to <code>.afm</code> files, can be directly opened in ChimeraX without requiring additional software installation.</p> <p>The deposited <code>.afm</code> file follows the 'AFM1' (metacode) format standard.</p>
3D localization AFM (3D-LAFM) density map of glutamate transporter GltPh inward facing state open (IFSopen) conformation at apo condition, imaged from the cytoplasmic side
<p>3D localization AFM (3D-LAFM) density map of glutamate transporter GltPh inward facing state open (IFSopen) conformation at apo condition, imaged from the cytoplasmic side , in <code>.afm</code> format and in <code>.mrc</code> format.</p> <p>Note: The <code>.afm</code> file encodes details for constructing 3D-LAFM density maps and includes experimental conditions in its header. Using <code>.afm</code> files requires the additional installation of the AFM file encoder (available from <a href="https://github.com/rafaeljiang23/3D-LAFM/tree/main/ChimeraX-AfmFormat_v2">GitHub</a>). Once the relevant installation is complete, <code>.afm</code> files can be opened in ChimeraX via drag-and-drop. In contrast, <code>.mrc</code> files, which encode only the density values equivalent to <code>.afm</code> files, can be directly opened in ChimeraX without requiring additional software installation.</p> <p>The deposited <code>.afm</code> file follows the 'AFM1' (metacode) format standard.</p>
3D localization AFM (3D-LAFM) density map of glutamate transporter GltPh inward facing state open, kinetically locked, (IFSopen-1) conformation at apo condition, imaged from the cytoplasmic side
<p>3D localization AFM (3D-LAFM) density map of glutamate transporter GltPh inward facing state open, kinetically locked, (IFSopen-1) conformation at apo condition, imaged from the cytoplasmic side , in <code>.afm</code> format and in <code>.mrc</code> format.</p> <p>Note: The <code>.afm</code> file encodes details for constructing 3D-LAFM density maps and includes experimental conditions in its header. Using <code>.afm</code> files requires the additional installation of the AFM file encoder (available from <a href="https://github.com/rafaeljiang23/3D-LAFM/tree/main/ChimeraX-AfmFormat_v2">GitHub</a>). Once the relevant installation is complete, <code>.afm</code> files can be opened in ChimeraX via drag-and-drop. In contrast, <code>.mrc</code> files, which encode only the density values equivalent to <code>.afm</code> files, can be directly opened in ChimeraX without requiring additional software installation.</p> <p>The deposited <code>.afm</code> file follows the 'AFM1' (metacode) format standard.</p>
Sex-specific fear acquisition following early life stress is linked to amygdala and hippocampal purine and glutamate metabolism
<p>Motion tracking dataset used for the paper "<strong><em>Sex-specific fear acquisition following early life stress is linked to amygdala and hippocampal purine and glutamate metabolism</em></strong>", by Joeri Bordes et al.</p> <p><strong><span>Abstract</span></strong></p> <p>Early life stress (ELS) can negatively impact health, increasing the risk of stress-related disorders, such as post-traumatic stress disorder (PTSD). Importantly, PTSD disproportionately affects women, emphasizing the critical need to explore how sex differences influence the genetic and metabolic neurobiological pathways underlying trauma-related behaviors. This study uses the limited bedding and nesting (LBN) paradigm to model ELS and investigate its sex-specific effects on fear memory formation. Employing innovative unsupervised behavioral classification, the current study reveals distinct behavioral patterns associated with fear acquisition and retrieval in male and female mice following ELS. Females exposed to LBN display heightened active fear responses, contrasting with males. Furthermore, the study examined the crucial link between behavioral regulation and cellular metabolism in key brain regions involved in fear and stress processing. Sex-specific and stress-dependent alterations were observed in purine, pyrimidine, and glutamate metabolism within the basolateral amygdala, the dorsal hippocampus, and the ventral hippocampus. These findings provide crucial insights into the complex interplay between metabolic pathways, the neurobiological underpinnings of fear memory, and stress responses. Importantly, they emphasize the significance of considering sex-specific metabolic alterations when investigating stress-related disorders, opening potential avenues for the development of targeted interventions.</p>
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>
Structures of reaction intermediates of the NAAG hydrolysis by glutamate carboxypeptidase II
<p>Representative frames from the molecular dynamics simulations in the regions of minima along the reaction path calculated at the QM(PBE0-D3/6-31G**)/MM(AMBER) level.</p>
Nanoelectrochemistry reveals how soluble Aβ42 oligomers alter vesicular storage and release of glutamate
<p class="MsoNormal">Glutamate (Glu) is the major excitatory transmitter in the nervous system. Impairment of its vesicular release by β-amyloid (Aβ) oligomers is thought to participate in pathological processes leading to Alzheimer's disease (AD). However, it remains unclear whether <span>soluble </span>Aβ<sub>42</sub> oligomers affect intravesicular amounts of Glu or their release in the brain, or both. Measurements made in this work on single Glu varicosities with an amperometric nanowire Glu biosensor revealed that <span>soluble </span>Aβ<sub>42 </sub>oligomers first caused a dramatic increase in vesicular Glu storage and stimulation-induced release, accompanied by a high level of parallel spontaneous exocytosis, ultimately resulting in depletion of intravesicular Glu content and greatly reduced release. Molecular biology tools and mouse models of Aβ amyloidosis have further established that the transient hyperexcitation observed during the primary pathological stage is mediated by an altered behavior of vesicular glutamate transporter 1 (VGLUT1) responsible for transporting Glu into synaptic vesicles. Thereafter, an overexpression of Vti1a, a protein that maintains spontaneous release of neurotransmitters by selective interaction with <span>t</span>-SNAREs, resulted in a depletion of intravesicular Glu content, triggering advanced-stage neuronal malfunction. These findings are expected to open new perspectives for remediating Aβ<sub>42</sub>-induced neuronal hyperactivity and neuronal degeneration.</p>
Effects of Recombinant Human Glutamic Acid Decarboxylase on the Progression of Type 1 Diabetes in New Onset Subjects
ClinicalTrials.gov study NCT00529399. IPD Sharing: YES. Countries: 2. Publications: 7.
Lurasidone Effects on Tissue Glutamate in Schizophrenia
ClinicalTrials.gov study NCT02199743. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Glutamate for Metabolic Intervention in Coronary Surgery
ClinicalTrials.gov study NCT00489827. IPD Sharing: Not stated. Countries: 1. Publications: 34.
Inflammation-Induced CNS Glutamate Changes in Depression
ClinicalTrials.gov study NCT03004443. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Injections of Glutamic Acid Decarboxylase (GAD) for LADA Type of Diabetes
ClinicalTrials.gov study NCT04262479. IPD Sharing: NO. Countries: 2. Publications: 1.
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
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
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.