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000285253 1001_ $$aSarmadi, Kamyab$$b0
000285253 245__ $$aLRRC8-Mediated Glutamate Release from Astrocytes Is Not Increased During the Initiation of Experimental Temporal Lobe Epilepsy.
000285253 260__ $$aBasel$$bMolecular Diversity Preservation International$$c2026
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000285253 520__ $$aLRRC8 channels are volume-regulated anion channels (VRACs) activated by cellular swelling, which mediate regulatory volume decrease in many cell types. Recently, it has been shown that these channels contribute to the release of glutamate from astrocytes. Since enhanced extracellular glutamate concentrations produce hyperexcitability, and microdialysis revealed elevated levels of the transmitter in the brains of epileptic patients, we asked whether astroglial glutamate release through LRRC8/VRACs might contribute to the initiation of experimental temporal lobe epilepsy (TLE). Patch clamp, pharmacological, and single-cell transcript analyses were performed in the hippocampus of controls and mice with inducible deletion of LRRC8a in astrocytes. In addition, these mice were exposed to our unilateral intracortical kainate model of TLE. Tonic currents were recorded from CA1 pyramidal neurons as a measure of glutamate release. Our data show that neither expression of LRRC8a nor the amplitude of tonic currents was altered 4 h after status epilepticus-induced TLE. These findings do not suggest that increased astroglial glutamate release through LRRC8 channels contributes to the initiation of experimental TLE.
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000285253 650_7 $$2Other$$aSWELL1
000285253 650_7 $$2Other$$aVRAC
000285253 650_7 $$2Other$$aVSOR
000285253 650_7 $$2Other$$aastrocyte
000285253 650_7 $$2Other$$achloride channel
000285253 650_7 $$2Other$$aepilepsy
000285253 650_7 $$03KX376GY7L$$2NLM Chemicals$$aGlutamic Acid
000285253 650_7 $$2NLM Chemicals$$aMembrane Proteins
000285253 650_7 $$0SIV03811UC$$2NLM Chemicals$$aKainic Acid
000285253 650_2 $$2MeSH$$aAstrocytes: metabolism
000285253 650_2 $$2MeSH$$aAnimals
000285253 650_2 $$2MeSH$$aEpilepsy, Temporal Lobe: metabolism
000285253 650_2 $$2MeSH$$aEpilepsy, Temporal Lobe: pathology
000285253 650_2 $$2MeSH$$aGlutamic Acid: metabolism
000285253 650_2 $$2MeSH$$aMice
000285253 650_2 $$2MeSH$$aDisease Models, Animal
000285253 650_2 $$2MeSH$$aMembrane Proteins: metabolism
000285253 650_2 $$2MeSH$$aMembrane Proteins: genetics
000285253 650_2 $$2MeSH$$aMale
000285253 650_2 $$2MeSH$$aKainic Acid
000285253 650_2 $$2MeSH$$aMice, Inbred C57BL
000285253 650_2 $$2MeSH$$aPyramidal Cells: metabolism
000285253 650_2 $$2MeSH$$aHippocampus: metabolism
000285253 7001_ $$aGaspar, Linda$$b1
000285253 7001_ $$00000-0003-0090-7553$$aBedner, Peter$$b2
000285253 7001_ $$00000-0003-4749-5162$$aHenning, Lukas$$b3
000285253 7001_ $$0P:(DE-2719)2811625$$aHenneberger, Christian$$b4
000285253 7001_ $$00000-0001-6612-7678$$aJabs, Ronald$$b5
000285253 7001_ $$00000-0002-3509-2553$$aJentsch, Thomas J$$b6
000285253 7001_ $$00000-0003-2579-8357$$aSteinhäuser, Christian$$b7
000285253 7001_ $$aSeifert, Gerald$$b8
000285253 770__ $$aRole of Glia in Human Health and Disease
000285253 773__ $$0PERI:(DE-600)2019364-6$$a10.3390/ijms27031589$$gVol. 27, no. 3, p. 1589 -$$n3$$p1589$$tInternational journal of molecular sciences$$v27$$x1422-0067$$y2026
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