DOI: 10.5061/dryad.qjq2bvqr1
title: Data from: Bidirectional dysregulation of synaptic glutamate signaling after transient metabolic failure

description: Ischemia leads to a severe dysregulation of glutamate homeostasis and
 excitotoxic cell damage in the brain. Shorter episodes of energy
 depletion, for instance during peri-infarct depolarizations, can also
 acutely perturb glutamate signaling. It is less clear if such episodes of
 metabolic failure also have persistent effects on glutamate signaling and
 how the relevant mechanisms such as glutamate release and uptake are
 differentially affected. We modeled acute and transient metabolic failure
 by using a chemical ischemia protocol and analyzed its effect on
 glutamatergic synaptic transmission and extracellular glutamate signals by
 electrophysiology and multiphoton imaging, respectively, in the mouse
 hippocampus. Our experiments uncover a duration-dependent bidirectional
 dysregulation of glutamate signaling. Whereas short chemical ischemia
 induces a lasting potentiation of presynaptic glutamate release and
 synaptic transmission, longer episodes result in a persistent postsynaptic
 failure of synaptic transmission. We also observed unexpected differences
 in the vulnerability of the investigated cellular mechanisms. Axonal
 action potential firing and glutamate uptake were surprisingly resilient
 compared to postsynaptic cells, which overall were most vulnerable to
 acute and transient metabolic stress. We conclude that even short
 perturbations of energy supply lead to a lasting potentiation of synaptic
 glutamate release, which may increase glutamate excitotoxicity well beyond
 the metabolic incident.
description: See manuscript by Passlick et al. for a complete description of
 data acquisition and analysis.
description: # Bidirectional dysregulation of synaptic glutamate signaling after
 transient metabolic failure
 [https://doi.org/10.5061/dryad.qjq2bvqr1](https://doi.org/10.5061/dryad.qjq2bvqr1) ## Description of the data and file structure from The data set contains the main experimental results from the article (primary work, see above), also indicated below. Please see there for a detailed description of data acquisition, analysis, interpretation and discussion. A previous version of the manuscript is also available on bioRxiv ([https://www.biorxiv.org/content/10.1101/2024.04.11.588988v2](https://www.biorxiv.org/content/10.1101/2024.04.11.588988v2)). **Bidirectional dysregulation of synaptic glutamate signaling after transient metabolic failure** Stefan Passlick 1, Ghanim Ullah 2, Christian Henneberger 1, 3, * 1 Institute of Cellular Neurosciences, Medical Faculty, University of Bonn, Bonn, Germany, 2 Department of Physics, University of South Florida, Tampa, FL 33620, USA, 3 German Center for Neurodegenerative Diseases, Bonn, Germany ### Files #### File: Fig1.xlsx **Description:** Contains data of figure panels 1G, 1H and 1I describing the effect of transient chemical ischemia on the axonal fiber volley (Fig. 1H) and fEPSP slope (Fig. 1G) and the relationship between peak [K+] during chemical ischemia and its effect on the fEPSP slope (Fig. 1I). All experimental conditions are indicated in the file. Individual numbers correspond to measurements from separate recordings. For more information, please see figure legend in the article and the article itself/bioRxiv manuscript (see above). #### File: Fig2.xlsx **Description:** Contains data of figure panels 2F, 2G and 2H corresponding to control experiments, experiments with chemical ischemia and chemical ischemia with postsynaptic failure, respectively. Analysed parameters (fiber volley, fEPSP slope, iGluSnFR dF/F0, iGluSnFR F0) are indicated in the individual data sheets. All effects are expressed relative to baseline recordings (at the beginning of the experiment). Individual numbers correspond to measurements from separate recordings. For more information, please see figure legend in the article and the article itself/bioRxiv manuscript (see above). #### File: Fig3.xlsx **Description:** Contains data of figure panels 3B, 3E, 3F and 3G describing the effect of transient chemical ischemia on iGluSnFR decay time constants (in ms) or control recordings obtained using paired stimuli (3B) or high-frequency stimulation (3E, 3F, 3G). All experimental conditions are indicated in the individual data sheets. Individual numbers correspond to measurements from separate recordings. For further information, please see figure legend in the article and the article itself/bioRxiv manuscript (see above). #### File: Fig4.xlsx **Description:** Conatins data underlying figure panels 4C and 4E quantifying the effect of chemical ischemia (without postsynaptic failure, CI) on the inhibitory effect of gDGG of evoked synaptic currents (EPSCs) and potentials (EPSPs) (4C) and on the axonal figure volley (4E). For each individual data sheet, the analysed parameters and experimental group (control or CI) are indicated. Individual numbers correspond to measurements from separate recordings. For further information, please see figure legend in the article and the article itself/bioRxiv manuscript (see above).