Home > In process > LRRC8-Mediated Glutamate Release from Astrocytes Is Not Increased During the Initiation of Experimental Temporal Lobe Epilepsy. > print

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024 7 _ |a 10.3390/ijms27031589
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024 7 _ |a 1422-0067
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024 7 _ |a 1661-6596
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037 _ _ |a DZNE-2026-00195
041 _ _ |a English
082 _ _ |a 540
100 1 _ |a Sarmadi, Kamyab
|b 0
245 _ _ |a LRRC8-Mediated Glutamate Release from Astrocytes Is Not Increased During the Initiation of Experimental Temporal Lobe Epilepsy.
260 _ _ |a Basel
|c 2026
|b Molecular Diversity Preservation International
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520 _ _ |a 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.
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650 _ 7 |a SWELL1
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650 _ 7 |a VRAC
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650 _ 7 |a VSOR
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650 _ 7 |a astrocyte
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650 _ 7 |a chloride channel
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650 _ 7 |a epilepsy
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650 _ 7 |a Glutamic Acid
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650 _ 7 |a Membrane Proteins
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650 _ 7 |a Kainic Acid
|0 SIV03811UC
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650 _ 2 |a Astrocytes: metabolism
|2 MeSH
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Epilepsy, Temporal Lobe: metabolism
|2 MeSH
650 _ 2 |a Epilepsy, Temporal Lobe: pathology
|2 MeSH
650 _ 2 |a Glutamic Acid: metabolism
|2 MeSH
650 _ 2 |a Mice
|2 MeSH
650 _ 2 |a Disease Models, Animal
|2 MeSH
650 _ 2 |a Membrane Proteins: metabolism
|2 MeSH
650 _ 2 |a Membrane Proteins: genetics
|2 MeSH
650 _ 2 |a Male
|2 MeSH
650 _ 2 |a Kainic Acid
|2 MeSH
650 _ 2 |a Mice, Inbred C57BL
|2 MeSH
650 _ 2 |a Pyramidal Cells: metabolism
|2 MeSH
650 _ 2 |a Hippocampus: metabolism
|2 MeSH
700 1 _ |a Gaspar, Linda
|b 1
700 1 _ |a Bedner, Peter
|0 0000-0003-0090-7553
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700 1 _ |a Henning, Lukas
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700 1 _ |a Henneberger, Christian
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700 1 _ |a Jabs, Ronald
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700 1 _ |a Jentsch, Thomas J
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700 1 _ |a Steinhäuser, Christian
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700 1 _ |a Seifert, Gerald
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770 _ _ |a Role of Glia in Human Health and Disease
773 _ _ |a 10.3390/ijms27031589
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910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
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