Anion transport in astrocytes.
We have examined the question of anion-transport systems in glia using primary astrocyte cultures prepared from neonatal rat brains. These studies show that these cells have exchange or cotransport systems for Cl- that appear to be electrically neutral, that is, SITS-sensitive Cl-/Cl- or Cl-/HCO3- anion exchange, and furosemide- and bumetanide-sensitive Na+ + K+ + 2Cl- cotransport. These inhibitors inhibit a major component of the total 36Cl- flux and the remaining Cl- flux may be conductive; however, this conductive flux makes a small contribution to Em relative to K+, since large changes in [Cl-]o do not usually affect Em, which is predominantly a K+ diffusion potential. We have also found an alpha-receptor-mediated depolarization that is affected by imposed changes in Ecl. The alpha-receptor-mediated depolarization seen at normal [Cl-]o could be partially due to increased Cl- conductance because [Cl-]i appears to be several-fold higher than it would be if it were in equilibrium with the membrane potential.
D000818:Animals; D000838:Anions / Q000378:metabolism*; D001253:Astrocytes / Q000378:metabolism*; D001639:Bicarbonates / Q000378:metabolism; D001921:Brain / Q000378:metabolism; D002245:Carbon Dioxide / Q000378:metabolism; D002352:Carrier Proteins / Q000378:metabolism*; D002478:Cells, Cultured; D002712:Chlorides / Q000378:metabolism; D006863:Hydrogen-Ion Concentration; D008564:Membrane Potentials; D008565:Membrane Proteins; D051381:Rats; D028021:Sodium-Potassium-Chloride Symporters
D000838:Anions; D001639:Bicarbonates; D002352:Carrier Proteins; D002712:Chlorides; D008565:Membrane Proteins; D028021:Sodium-Potassium-Chloride Symporters; D002245:Carbon Dioxide