ACUTE AND CHRONIC EFFECTS OF POTASSIUM AND NORADRENALINE ON NA-ATPASEACTIVITY IN CULTURED MOUSE NEURONS AND ASTROCYTES()

Acute and chronic effects of elevated extracellular concentrations of potassium ions ([K+](0)) and/or noradrenaline were studied in homogena tes of primary cultures of mouse astrocytes, from the cerebral cortex or the spinal cord, and of. primary cultures of mouse cerebral cortica l neurons. Na+, K+- ATPase activity in cerebral cortical astrocytes sh owed a K-m value of 1.9 mM with confidence limits of 1.3-2.9 mM and a V-max of 5.4 mu mol/h/mg protein with confidence limits of 3.3-8.1 mu mol/h/mg protein. Due to the high K-m value, the activity of the enzym e was significantly increased by an increase in [K+](0) in the interva l 5-12 mM. In cerebral cortical neurons, V-max was lower (1.77+/-0.06 mu mol/h/mg protein) but the affinity was higher (K-m 0.43+/-0.8 mM). With these kinetics, there is no stimulation of enzyme activity when [ K+](0) is increased beyond control levels. In spinal cord astrocytes, the relative effect of increasing IK+](0) above 6 mM was larger than i n cerebral astrocytes but the absolute activity of the enzyme was lowe r. Na+, K+-ATPase activity in both types of astrocyte was stimulated b y noradrenaline and its beta-adrenergic subtype agonist isoproterenol but mainly or exclusively at 6 mM [K+](0) Noradrenaline also caused a stimulation in cortical neurons, but at non-physiological K+ concentra tions this stimulation was converted to an inhibition, and isoproteren ol had no stimulatory effect. Chronic exposure of cerebral cortical as trocytes to elevated [K+](0) caused a decrease in Na+, K+-ATPase activ ity when enzyme activity in the cells was subsequently measured at nor mal [K+](0) During exposure to 30 mM [K+](0) this ''down regulation'' took place within 10 min. Conversely, chronic exposure to reduced [K+] (0) led to an increase in Na+, K+-ATPase activity. Chronic exposure to noradrenaline had no significant effect but there was a tendency towa rds an increase.