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@ARTICLE{Sarmadi:285253,
      author       = {Sarmadi, Kamyab and Gaspar, Linda and Bedner, Peter and
                      Henning, Lukas and Henneberger, Christian and Jabs, Ronald
                      and Jentsch, Thomas J and Steinhäuser, Christian and
                      Seifert, Gerald},
      title        = {{LRRC}8-{M}ediated {G}lutamate {R}elease from {A}strocytes
                      {I}s {N}ot {I}ncreased {D}uring the {I}nitiation of
                      {E}xperimental {T}emporal {L}obe {E}pilepsy.},
      journal      = {International journal of molecular sciences},
      volume       = {27},
      number       = {3},
      issn         = {1422-0067},
      address      = {Basel},
      publisher    = {Molecular Diversity Preservation International},
      reportid     = {DZNE-2026-00195},
      pages        = {1589},
      year         = {2026},
      abstract     = {LRRC8 channels are volume-regulated anion channels (VRACs)
                      activated by cellular swelling, which mediate regulatory
                      volume decrease in many cell types. Recently, it has been
                      shown that these channels contribute to the release of
                      glutamate from astrocytes. Since enhanced extracellular
                      glutamate concentrations produce hyperexcitability, and
                      microdialysis revealed elevated levels of the transmitter in
                      the brains of epileptic patients, we asked whether
                      astroglial glutamate release through LRRC8/VRACs might
                      contribute to the initiation of experimental temporal lobe
                      epilepsy (TLE). Patch clamp, pharmacological, and
                      single-cell transcript analyses were performed in the
                      hippocampus of controls and mice with inducible deletion of
                      LRRC8a in astrocytes. In addition, these mice were exposed
                      to our unilateral intracortical kainate model of TLE. Tonic
                      currents were recorded from CA1 pyramidal neurons as a
                      measure of glutamate release. Our data show that neither
                      expression of LRRC8a nor the amplitude of tonic currents was
                      altered 4 h after status epilepticus-induced TLE. These
                      findings do not suggest that increased astroglial glutamate
                      release through LRRC8 channels contributes to the initiation
                      of experimental TLE.},
      keywords     = {Astrocytes: metabolism / Animals / Epilepsy, Temporal Lobe:
                      metabolism / Epilepsy, Temporal Lobe: pathology / Glutamic
                      Acid: metabolism / Mice / Disease Models, Animal / Membrane
                      Proteins: metabolism / Membrane Proteins: genetics / Male /
                      Kainic Acid / Mice, Inbred C57BL / Pyramidal Cells:
                      metabolism / Hippocampus: metabolism / SWELL1 (Other) / VRAC
                      (Other) / VSOR (Other) / astrocyte (Other) / chloride
                      channel (Other) / epilepsy (Other) / Glutamic Acid (NLM
                      Chemicals) / Membrane Proteins (NLM Chemicals) / Kainic Acid
                      (NLM Chemicals)},
      cin          = {AG Henneberger},
      ddc          = {540},
      cid          = {I:(DE-2719)1013029},
      pnm          = {351 - Brain Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41684009},
      pmc          = {pmc:PMC12898268},
      doi          = {10.3390/ijms27031589},
      url          = {https://pub.dzne.de/record/285253},
}