Journal Article

DZNE-2026-00195

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png LRRC8-Mediated Glutamate Release from Astrocytes Is Not Increased During the Initiation of Experimental Temporal Lobe Epilepsy.

Sarmadi, K. ; Gaspar, L. ; Bedner, P. ; Henning, L. ; Henneberger, C.DZNE* ; Jabs, R. ; Jentsch, T. J. ; Steinhäuser, C. ; Seifert, G.

2026
Molecular Diversity Preservation International Basel

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Please use a persistent id in citations: doi:10.3390/ijms27031589

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.

Keyword(s): Astrocytes: metabolism (MeSH) ; Animals (MeSH) ; Epilepsy, Temporal Lobe: metabolism (MeSH) ; Epilepsy, Temporal Lobe: pathology (MeSH) ; Glutamic Acid: metabolism (MeSH) ; Mice (MeSH) ; Disease Models, Animal (MeSH) ; Membrane Proteins: metabolism (MeSH) ; Membrane Proteins: genetics (MeSH) ; Male (MeSH) ; Kainic Acid (MeSH) ; Mice, Inbred C57BL (MeSH) ; Pyramidal Cells: metabolism (MeSH) ; Hippocampus: metabolism (MeSH) ; SWELL1 ; VRAC ; VSOR ; astrocyte ; chloride channel ; epilepsy ; Glutamic Acid ; Membrane Proteins ; Kainic Acid

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Contributing Institute(s):

1. Synaptic and Glial Plasticity (AG Henneberger)

Research Program(s):

1. 351 - Brain Function (POF4-351) (POF4-351)

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Database coverage:
; Clarivate Analytics Master Journal List ; Current Contents - Physical, Chemical and Earth Sciences ; Ebsco Academic Search ; Essential Science Indicators ; IF >= 5 ; JCR ; PubMed Central ; SCOPUS ; Science Citation Index Expanded ; Web of Science Core Collection

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