title: Astrocytes from mouse brain slices express ClC-2-mediated Cl- currents regulated during development and after injury.
abstract: Chloride channels are important for astrocytic volume regulation and K+ buffering. We demonstrate functional expression of a hyperpolarization-activated Cl- current in a subpopulation of astrocytes in acute slices or after fresh isolation from adult brain of GFAP/EGFP transgenic animals in which astrocytes are selectively labeled. When Na+ and K+ were substituted with NMDG+ and Cs+ in extra- and intracellular solutions, an inward current was observed at negative membrane potentials. The current displayed features as described for a Cl- current characterized in cultured astrocytes: it activated time dependently at potentials negative to -40 mV, displayed no inactivation within 1 s, and was inhibited reversibly by submicromolar concentrations of Cd2+. The current was not detectable in astrocytes from ClC-2 knockout mice, indicating that the ClC-2 chloride channel generated the conductance. Current density was significantly lower in a corresponding population of astrocytes isolated from immature brain and in reactive astrocytes within a lesion site.
authors.affiliation: Department of Physiology and Laboratory of Cellular and Molecular Physiology, Semmelweis University Medical School, Budapest, Hungary.
authors.forename: Judit K
authors.initials: JK
authors.lastname: Makara
authors.forename: Angelika
authors.initials: A
authors.lastname: Rappert
authors.forename: Katja
authors.initials: K
authors.lastname: Matthias
authors.forename: Christian
authors.initials: C
authors.lastname: Steinhäuser
authors.forename: András
authors.initials: A
authors.lastname: Spät
authors.forename: Helmut
authors.initials: H
authors.lastname: Kettenmann
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D001921:Brain / Q000166:cytology / Q000254:growth & development* / Q000378:metabolism*; D001930:Brain Injuries / Q000235:genetics / Q000378:metabolism*; D000090007:CLC-2 Chloride Channels; D002104:Cadmium / Q000494:pharmacology; D002462:Cell Membrane / Q000187:drug effects / Q000378:metabolism*; D002540:Cerebral Cortex / Q000166:cytology / Q000254:growth & development / Q000378:metabolism; D002586:Cesium / Q000494:pharmacology; D018118:Chloride Channels / Q000172:deficiency* / Q000235:genetics; D002712:Chlorides / Q000378:metabolism; D018507:Gene Expression Regulation, Developmental / Q000235:genetics; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D005911:Gliosis / Q000235:genetics / Q000378:metabolism; D049452:Green Fluorescent Proteins; D006624:Hippocampus / Q000166:cytology / Q000254:growth & development / Q000378:metabolism; D008164:Luminescent Proteins; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D051379:Mice; D018345:Mice, Knockout; D008822:Mice, Transgenic; D009924:Organ Culture Techniques
chemical_list: D000090007:CLC-2 Chloride Channels; D018118:Chloride Channels; D002712:Chlorides; D005904:Glial Fibrillary Acidic Protein; D008164:Luminescent Proteins; D002104:Cadmium; D049452:Green Fluorescent Proteins; D002586:Cesium