Abstract

42K and 22Na contents and unidirectional fluxes, as well as net accumulation of 42K in response to elevated extracellular K +, were investigated in primary cultures of astrocytes prepared from neonatal rat and mouse brain. The major difference between both species affected the unidirectional K + influx which was up to 75 times higher in mouse as compared to rat cultures. The flux rates in mouse astrocytes were doubled by measuring uptake in salt solution instead of growth medium, while 42K influx in rat astrocytes was unaffected by such treatment. 22Na transport was very similar in astrocytes from both species. The length of culture period and treatment with DBcAMP (2′,3′-dibutyryl cyclic adenyl monophosphate) modified K + transport but not Na + transport. Both types of cultures showed the same accumulation of 42K in response to raised medium K +. Amiloride inhibited 42K influx by 41% and 13% in mouse and rat cultures, respectively. In contrast, furosemide inhibited 42K uptake in rat astrocytes cultures by 50% but had no effect on mouse astrocyte cultures. 50 μM barium chloride markedly inhibited 42K uptake in mouse cultures by 96% (or 1491 nmol·mg −1·min −1), but inhibited 42K uptake in rat cultures by only 23% (or 9 nmol·mg −1·min −1). Ouabain was similarly effective in both types of astrocyte cultures. We conclude that Na + transport as well as net K + accumulation and Cl − transport (based on previous studies) properties are reasonably stable and reproduced in primary cultures from both mouse and rat brain. However, unidirectional K + influx showed a large species difference and also a larger variation due to differences in culturing conditions. There were also differences in the sensitivity to some inhibitors. Possible causes could be differences in the number or characteristics of K + channels as well as other specific K + transport systems.

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