000272155 001__ 272155
000272155 005__ 20250127091531.0
000272155 0247_ $$2pmc$$apmc:PMC11407764
000272155 0247_ $$2doi$$a10.7554/eLife.98834
000272155 0247_ $$2pmid$$apmid:39287515
000272155 0247_ $$2altmetric$$aaltmetric:167944511
000272155 037__ $$aDZNE-2024-01146
000272155 041__ $$aEnglish
000272155 082__ $$a600
000272155 1001_ $$00000-0002-7703-7018$$aPasslick, Stefan$$b0
000272155 245__ $$aBidirectional dysregulation of synaptic glutamate signaling after transient metabolic failure.
000272155 260__ $$aCambridge$$beLife Sciences Publications$$c2024
000272155 3367_ $$2DRIVER$$aarticle
000272155 3367_ $$2DataCite$$aOutput Types/Journal article
000272155 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1727165422_25599
000272155 3367_ $$2BibTeX$$aARTICLE
000272155 3367_ $$2ORCID$$aJOURNAL_ARTICLE
000272155 3367_ $$00$$2EndNote$$aJournal Article
000272155 520__ $$aIschemia 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 short perturbations of energy supply lead to a lasting potentiation of synaptic glutamate release, which may increase glutamate excitotoxicity well beyond the metabolic incident.
000272155 536__ $$0G:(DE-HGF)POF4-351$$a351 - Brain Function (POF4-351)$$cPOF4-351$$fPOF IV$$x0
000272155 588__ $$aDataset connected to CrossRef, PubMed, , Journals: pub.dzne.de
000272155 650_7 $$2Other$$aglutamate release
000272155 650_7 $$2Other$$aglutamate uptake
000272155 650_7 $$2Other$$aischemia
000272155 650_7 $$2Other$$ametabolic failure
000272155 650_7 $$2Other$$amouse
000272155 650_7 $$2Other$$aneuroscience
000272155 650_7 $$2Other$$astroke
000272155 650_7 $$2Other$$asynaptic transmission
000272155 650_7 $$03KX376GY7L$$2NLM Chemicals$$aGlutamic Acid
000272155 650_2 $$2MeSH$$aAnimals
000272155 650_2 $$2MeSH$$aGlutamic Acid: metabolism
000272155 650_2 $$2MeSH$$aMice
000272155 650_2 $$2MeSH$$aSynaptic Transmission
000272155 650_2 $$2MeSH$$aHippocampus: metabolism
000272155 650_2 $$2MeSH$$aSignal Transduction
000272155 650_2 $$2MeSH$$aMale
000272155 650_2 $$2MeSH$$aSynapses: metabolism
000272155 650_2 $$2MeSH$$aSynapses: physiology
000272155 650_2 $$2MeSH$$aMice, Inbred C57BL
000272155 7001_ $$aUllah, Ghanim$$b1
000272155 7001_ $$0P:(DE-2719)2811625$$aHenneberger, Christian$$b2$$eLast author
000272155 773__ $$0PERI:(DE-600)2687154-3$$a10.7554/eLife.98834$$gVol. 13, p. RP98834$$pRP98834$$teLife$$v13$$x2050-084X$$y2024
000272155 8564_ $$uhttps://pub.dzne.de/record/272155/files/DZNE-2024-01146%20SUP.pdf
000272155 8564_ $$uhttps://pub.dzne.de/record/272155/files/DZNE-2024-01146.pdf$$yOpenAccess
000272155 8564_ $$uhttps://pub.dzne.de/record/272155/files/DZNE-2024-01146%20SUP.pdf?subformat=pdfa$$xpdfa
000272155 8564_ $$uhttps://pub.dzne.de/record/272155/files/DZNE-2024-01146.pdf?subformat=pdfa$$xpdfa$$yOpenAccess
000272155 909CO $$ooai:pub.dzne.de:272155$$pdnbdelivery$$pdriver$$pVDB$$popen_access$$popenaire
000272155 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)2811625$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b2$$kDZNE
000272155 9131_ $$0G:(DE-HGF)POF4-351$$1G:(DE-HGF)POF4-350$$2G:(DE-HGF)POF4-300$$3G:(DE-HGF)POF4$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lNeurodegenerative Diseases$$vBrain Function$$x0
000272155 9141_ $$y2024
000272155 915__ $$0StatID:(DE-HGF)0200$$2StatID$$aDBCoverage$$bSCOPUS$$d2023-08-22
000272155 915__ $$0StatID:(DE-HGF)0160$$2StatID$$aDBCoverage$$bEssential Science Indicators$$d2023-08-22
000272155 915__ $$0StatID:(DE-HGF)1050$$2StatID$$aDBCoverage$$bBIOSIS Previews$$d2023-08-22
000272155 915__ $$0StatID:(DE-HGF)1190$$2StatID$$aDBCoverage$$bBiological Abstracts$$d2023-08-22
000272155 915__ $$0StatID:(DE-HGF)0600$$2StatID$$aDBCoverage$$bEbsco Academic Search$$d2023-08-22
000272155 915__ $$0StatID:(DE-HGF)1040$$2StatID$$aDBCoverage$$bZoological Record$$d2023-08-22
000272155 915__ $$0StatID:(DE-HGF)0100$$2StatID$$aJCR$$bELIFE : 2022$$d2023-08-22
000272155 915__ $$0StatID:(DE-HGF)0501$$2StatID$$aDBCoverage$$bDOAJ Seal$$d2022-09-23T12:20:44Z
000272155 915__ $$0StatID:(DE-HGF)0500$$2StatID$$aDBCoverage$$bDOAJ$$d2022-09-23T12:20:44Z
000272155 915__ $$0StatID:(DE-HGF)0113$$2StatID$$aWoS$$bScience Citation Index Expanded$$d2023-08-22
000272155 915__ $$0StatID:(DE-HGF)0700$$2StatID$$aFees$$d2023-08-22
000272155 915__ $$0StatID:(DE-HGF)0150$$2StatID$$aDBCoverage$$bWeb of Science Core Collection$$d2023-08-22
000272155 915__ $$0LIC:(DE-HGF)CCBY4$$2HGFVOC$$aCreative Commons Attribution CC BY 4.0
000272155 915__ $$0StatID:(DE-HGF)0510$$2StatID$$aOpenAccess
000272155 915__ $$0StatID:(DE-HGF)0030$$2StatID$$aPeer Review$$bASC$$d2023-08-22
000272155 915__ $$0StatID:(DE-HGF)0561$$2StatID$$aArticle Processing Charges$$d2023-08-22
000272155 915__ $$0StatID:(DE-HGF)9905$$2StatID$$aIF >= 5$$bELIFE : 2022$$d2023-08-22
000272155 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline$$d2023-08-22
000272155 915__ $$0StatID:(DE-HGF)0320$$2StatID$$aDBCoverage$$bPubMed Central$$d2023-08-22
000272155 915__ $$0StatID:(DE-HGF)0199$$2StatID$$aDBCoverage$$bClarivate Analytics Master Journal List$$d2023-08-22
000272155 9201_ $$0I:(DE-2719)1013029$$kAG Henneberger$$lSynaptic and Glial Plasticity$$x0
000272155 980__ $$ajournal
000272155 980__ $$aVDB
000272155 980__ $$aUNRESTRICTED
000272155 980__ $$aI:(DE-2719)1013029
000272155 9801_ $$aFullTexts