IMMATURE STAGE OF INTRACELLULAR CL^- HOMEOSTASIS BY CATION-CL^- COTRANSPORTERS IN RAT NEOCORTICAL NEURONS

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In brain slices from rat somatosesory cortex, neuronal intracellular Cl^- concentration ([Cl^-]_i) recordings were made by an optical technique measuring 6-methoxy-N-ethlquinolinium iodide (MEQ) fluorescence. When the resting [Cl^-]_i was estimated by calibration curve according to Stern-Volmer relationship, the [Cl^-]_i from postnatal day (P) 10-14 slices was significantly higher than that from P17-19 slices. Then, P10-14 slices were pretreated with inhibitors of cation-Cl^- cotranspoters to clarify the type that is responsible for the high [Cl^-]_i status. Furosemide did not alter this higher levels of [Cl^-]_i, whereas bumetanide significantly decreased it. Application of γ-aminobutyric acid (GABA) induced Cl^- efflux in most cortical neurons during P10-14. These results suggest that inwardly directed cation-Cl^- cotransporter, possibily bumetanide-sensitive Na^+, K^+-2Cl^- cotransporter, contributes to this intracellular Cl^- accumulation. Such an immature stage of Cl^- homeostasis would result in the reversal of the action of GABA in immature neurons as compared with mature ones.
名古屋市立大学の論文
2000-03-31