Acute and chronic effects of potassium and noradrenaline on Na +, K +-ATPase activity in cultured mouse neurons and astrocytes

• Published in: Neurochemistry international 1996-03, Vol.28 (3), p.335-342
• Main Authors: Hajek, Ivan, Subbarao, Kala V.S., Hertz, Leif
• Format: Article
• Language: English
• Subjects: Adrenergic alpha-Agonists - pharmacology; Animals; Astrocytes - drug effects; Astrocytes - enzymology; Biological and medical sciences; Cells, Cultured; Cerebral Cortex - cytology; Cerebral Cortex - drug effects; Cerebral Cortex - metabolism; Fundamental and applied biological sciences. Psychology; Isolated neuron and nerve. Neuroglia; Kinetics; Mice; Neurons - drug effects; Neurons - enzymology; Norepinephrine - pharmacology; Potassium - pharmacology; Sodium-Potassium-Exchanging ATPase - antagonists & inhibitors; Sodium-Potassium-Exchanging ATPase - metabolism; Spinal Cord - cytology; Spinal Cord - drug effects; Spinal Cord - metabolism; Stimulation, Chemical; Vertebrates: nervous system and sense organs
• ISSN: 0197-0186; 1872-9754
• DOI: 10.1016/0197-0186(95)00081-X

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 K m value of 1.9 mM with confidence limits of 1.3–2.9 mM and a V max of 5.4 μmol/h/mg protein with confidence limits of 3.3–8.1 μmol/h/mg protein. Due to the high K m 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, V max was lower (1.77±0.06 μmol/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 [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 β-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.