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@ARTICLE{Gerkau:874176,
      author       = {Gerkau, Niklas J. and Lerchundi, Rodrigo and Nelson, Joel
                      S. E. and Lantermann, Marina and Meyer, Jan and Hirrlinger,
                      Johannes and Rose, Christine R.},
      title        = {{R}elation between activity‐induced intracellular sodium
                      transients and {ATP} dynamics in mouse hippocampal neurons},
      journal      = {The journal of physiology},
      volume       = {597},
      number       = {23},
      issn         = {1469-7793},
      address      = {Hoboken, NJ},
      publisher    = {Wiley-Blackwell},
      reportid     = {FZJ-2020-01276},
      pages        = {5687 - 5705},
      year         = {2019},
      abstract     = {Excitatory neuronal activity results in the influx of Na+
                      through voltage‐ and ligand‐gated channels. Recovery
                      from accompanying increases in intracellular Na+
                      concentrations ([Na+]i) is mainly mediated by the
                      Na+/K+‐ATPase (NKA) and is one of the major
                      energy‐consuming processes in the brain. Here, we analysed
                      the relation between different patterns of
                      activity‐induced [Na+]i signalling and ATP in mouse
                      hippocampal CA1 pyramidal neurons by Na+ imaging with
                      sodium‐binding benzofurane isophthalate (SBFI) and
                      employing the genetically encoded nanosensor ATeam1.03YEMK
                      (ATeam). In situ calibrations demonstrated a sigmoidal
                      dependence of the ATeam Förster resonance energy transfer
                      ratio on the intracellular ATP concentration ([ATP]i) with
                      an apparent KD of 2.6 mm, indicating its suitability for
                      [ATP]i measurement. Induction of recurrent network activity
                      resulted in global [Na+]i oscillations with amplitudes of
                      ∼10 mm, encompassing somata and dendrites. These were
                      accompanied by a steady decline in [ATP]i by 0.3–0.4 mm in
                      both compartments. Global [Na+]i transients, induced by
                      afferent fibre stimulation or bath application of glutamate,
                      caused delayed, transient decreases in [ATP]i as well. Brief
                      focal glutamate application that evoked transient local Na+
                      influx into a dendrite, however, did not result in a
                      measurable reduction in [ATP]i. Our results suggest that ATP
                      consumption by the NKA following global [Na+]i transients
                      temporarily overrides its availability, causing a decrease
                      in [ATP]i. Locally restricted Na+ transients, however, do
                      not result in detectable changes in local [ATP]i, suggesting
                      that ATP production, together with rapid intracellular
                      diffusion of both ATP and Na+ from and to unstimulated
                      neighbouring regions, counteracts a local energy shortage
                      under these conditions.},
      cin          = {IHRS-BioSoft / ICS-4},
      ddc          = {610},
      cid          = {I:(DE-Juel1)IHRS-BioSoft-20161118 /
                      I:(DE-Juel1)ICS-4-20110106},
      pnm          = {553 - Physical Basis of Diseases (POF3-553) / IHRS-BioSoft
                      - International Helmholtz Research School of Biophysics and
                      Soft Matter (IHRS-BioSoft-20061101)},
      pid          = {G:(DE-HGF)POF3-553 / G:(DE-Juel1)IHRS-BioSoft-20061101},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:31549401},
      UT           = {WOS:000493167900001},
      doi          = {10.1113/JP278658},
      url          = {https://juser.fz-juelich.de/record/874176},
}