Carrier-mediated Cl transport in cultured mouse oligodendrocytes

Authors

  • D. Hoppe,

    1. Department of Neurobiology, Univer̀sity of Heidelberg, Heidelberg, Federal Republic of Germany
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  • H. Kettenmann

    Corresponding author
    1. Department of Neurobiology, Univer̀sity of Heidelberg, Heidelberg, Federal Republic of Germany
    • Department of Neurobiology, University of Heidelberg, Im Neuenheimer Feld 504, 6900-Heidelberg, F.R.G
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Abstract

We studied the steady state and the regulation of intracellular Cl activity (aCli) and the mechanisms of KCl uptake in cultured oligodendrocytes from mouse spinal cord using Cl-selective microelectrodes. The majority of oligodendrocytes actively accumulated Cl above passive distribution (2–3 mM), few cells showed a passive Cl distribution. To identify the carriers mediating Cl uptake, oligodendrocytes were maintained in a solution with low extracellular Cl concentration ([Cl]0) which resulted in a rapid decrease in aCli. The recovery of aCli above its passive distribution in normal [Cl]0 was blocked in the absence of Na+ or in the presence of furosemide and of bumetanide, which has been reported to inhibit Na+/K+/Cl cotransport. We therefore conclude that Cl uptake is primarily due to the activity of a Na+/K+/Cl transport system. Cl uptake above passive distribution was not affected in HCO3-free solution or in the presence of SITS and DIDS, indicating that Cl/HCO3 exchange is not involved in Cl uptake by oligodendrocytes. Elevation of [K+]0 induced an increase in aCli and, as shown earlier, intracellular K+ activity. This K+-induced Cl uptake was not blocked by bumetanide, furosemide, SITS, or DIDS, suggesting that under conditions of raised [K+]0 the combined uptake of K+ and Cl is not mediated by a carrier, but can be explained by the entry through channels driven by Donnan forces.

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