In:
American Journal of Physiology-Cell Physiology, American Physiological Society, Vol. 282, No. 5 ( 2002-05-01), p. C1147-C1160
Kurzfassung:
We reported previously that inhibition of Na + -K + -Cl − cotransporter isoform 1 (NKCC1) by bumetanide abolishes high extracellular K + concentration ([K + ] o )-induced swelling and intracellular Cl − accumulation in rat cortical astrocytes. In this report, we extended our study by using cortical astrocytes from NKCC1-deficient (NKCC1 −/− ) mice. NKCC1 protein and activity were absent in NKCC1 −/− astrocytes. [K + ] o of 75 mM increased NKCC1 activity approximately fourfold in NKCC1 +/+ cells ( P 〈 0.05) but had no effect in NKCC1 −/− astrocytes. Intracellular Cl − was increased by 70% in NKCC1 +/+ astrocytes under 75 mM [K + ] o ( P 〈 0.05) but remained unchanged in NKCC1 −/− astrocytes. Baseline intracellular Na + concentration ([Na + ] i ) in NKCC1 +/+ astrocytes was 19.0 ± 0.5 mM, compared with 16.9 ± 0.3 mM [Na + ] i in NKCC1 −/− astrocytes ( P 〈 0.05). Relative cell volume of NKCC1 +/+ astrocytes increased by 13 ± 2% in 75 mM [K + ] o , compared with a value of 1.0 ± 0.5% in NKCC1 −/− astrocytes ( P 〈 0.05). Regulatory volume increase after hypertonic shrinkage was completely impaired in NKCC1 −/− astrocytes. High-[K + ] o -induced 14 C-labeledd-aspartate release was reduced by ∼30% in NKCC1 −/− astrocytes. Our study suggests that stimulation of NKCC1 is required for high-[K + ] o -induced swelling, which contributes to glutamate release from astrocytes under high [K + ] o .
Materialart:
Online-Ressource
ISSN:
0363-6143
,
1522-1563
DOI:
10.1152/ajpcell.00538.2001
Sprache:
Englisch
Verlag:
American Physiological Society
Publikationsdatum:
2002
ZDB Id:
1477334-X
SSG:
12
