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@ARTICLE{Passlick:272155,
      author       = {Passlick, Stefan and Ullah, Ghanim and Henneberger,
                      Christian},
      title        = {{B}idirectional dysregulation of synaptic glutamate
                      signaling after transient metabolic failure.},
      journal      = {eLife},
      volume       = {13},
      issn         = {2050-084X},
      address      = {Cambridge},
      publisher    = {eLife Sciences Publications},
      reportid     = {DZNE-2024-01146},
      pages        = {RP98834},
      year         = {2024},
      abstract     = {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 short perturbations of energy supply lead to a
                      lasting potentiation of synaptic glutamate release, which
                      may increase glutamate excitotoxicity well beyond the
                      metabolic incident.},
      keywords     = {Animals / Glutamic Acid: metabolism / Mice / Synaptic
                      Transmission / Hippocampus: metabolism / Signal Transduction
                      / Male / Synapses: metabolism / Synapses: physiology / Mice,
                      Inbred C57BL / glutamate release (Other) / glutamate uptake
                      (Other) / ischemia (Other) / metabolic failure (Other) /
                      mouse (Other) / neuroscience (Other) / stroke (Other) /
                      synaptic transmission (Other) / Glutamic Acid (NLM
                      Chemicals)},
      cin          = {AG Henneberger},
      ddc          = {600},
      cid          = {I:(DE-2719)1013029},
      pnm          = {351 - Brain Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pmc          = {pmc:PMC11407764},
      pubmed       = {pmid:39287515},
      doi          = {10.7554/eLife.98834},
      url          = {https://pub.dzne.de/record/272155},
}