Carrier-mediated Cl− transport in cultured mouse oligodendrocytes

✍ Scribed by D. Hoppe; H. Kettenmann

• Publisher: John Wiley and Sons
• Year: 1989
• Tongue: English
• Weight: 731 KB
• Volume: 23
• Category: Article
• ISSN: 0360-4012
• DOI: 10.1002/jnr.490230415

✦ Synopsis

We studied the steady state and the regulation of intracellular C1-activity (aC1-i) and the mechanisms of KCI uptake in cultured oligodendrocytes from mouse spinal cord using CI--selective microelectrodes. The majority of oligodendrocytes actively accumulated C1-above passive distribution (2-3 mM), few cells showed a passive C1-distribution. To identify the carriers mediating C1-uptake, oligodendrocytes were maintained in a solution with low extracellular C1-concentration ([Cl-I,) which resulted in a rapid decrease in aC1-i. The recovery of aCFi above its passive distribution in normal [Cl-1, was blocked in the absence of Na+ or in the presence of furosemide and of bumetanide, which has been reported to inhibit Na+/K+/CI-cotransport. We therefore conclude that C1-uptake is primarily due to the activity of a Na+/K+/CI-transport system. C1-uptake above passive distribution was not affected in HC03--free solution or in the presence of SITS and DIDS, indicating that CI-/HC03-exchange is not involved in C1-uptake by oligodendrocytes. Elevation of [K+], induced an increase in aC1-i and, as shown earlier, intracellular K + activity. This K+-induced CI-uptake was not blocked by bumetanide, furosemide, SITS, or DIDS, suggesting that under conditions of raised [K+], the combined uptake of K + and C1-is not mediated by a carrier, but can be explained by the entry through channels driven by Donnan forces.