title: Acute and chronic effects of potassium and noradrenaline on Na+, K+-ATPase activity in cultured mouse neurons and astrocytes.
abstract: Acute and chronic effects of elevated extracellular concentrations of potassium ions ([K+]0) and/or noradrenaline were studied in homogenates of primary cultures of mouse astrocytes, from the cerebral cortex or the spinal cord, and of primary cultures of mouse cerebral cortical neurons. NA+, K+-ATPase activity in cerebral cortical astrocytes showed a Km value of 1.9 mM with confidence limits of 1.3-2.9 mM and a Vmax of 5.4 mumol/h/mg protein with confidence limits of 3.3-8.1 mumol/h/mg protein. Due to the high Km value, the activity of the enzyme was significantly increased by an increase in [K+]0 in the interval 5-12 mM. In cerebral cortical neurons, Vmax was lower (1.77 +/- 0.06 mumol/h/mg protein) but the affinity was higher (Km 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 [K+]0 above 6 mM was larger than in cerebral astrocytes but the absolute activity of the enzyme was lower. Na+, K+-ATPase activity in both types of astrocyte was stimulated by 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+ concentrations this stimulation was converted to an inhibition, and isoproterenol had no stimulatory effect. Chronic exposure of cerebral cortical astrocytes to elevated [K+]0 caused a decrease in Na+, K+-ATPase activity when enzyme activity in the cells was subsequently measured at normal [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 towards an increase.
authors.affiliation: Laboratory of Cellular Neurophysiology, Czech Academy of Sciences, Prague, The Czech Republic.
authors.forename: I
authors.initials: I
authors.lastname: Hajek
authors.forename: K V
authors.initials: KV
authors.lastname: Subbarao
authors.forename: L
authors.initials: L
authors.lastname: Hertz
mesh_terms: D000316:Adrenergic alpha-Agonists / Q000494:pharmacology*; D000818:Animals; D001253:Astrocytes / Q000187:drug effects / Q000201:enzymology*; D002478:Cells, Cultured; D002540:Cerebral Cortex / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D007700:Kinetics; D051379:Mice; D009474:Neurons / Q000187:drug effects / Q000201:enzymology*; D009638:Norepinephrine / Q000494:pharmacology*; D011188:Potassium / Q000494:pharmacology*; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors / Q000378:metabolism*; D013116:Spinal Cord / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D013268:Stimulation, Chemical
chemical_list: D000316:Adrenergic alpha-Agonists; D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium; D009638:Norepinephrine