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

Acute and chronic effects of potassium and noradrenaline on Na + , K + -ATPase activity in... 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. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Neurochemistry International Elsevier

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

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Publisher
Elsevier
Copyright
Copyright © 1996 Elsevier Ltd
ISSN
0197-0186
DOI
10.1016/0197-0186(95)00081-X
Publisher site
See Article on Publisher Site

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 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.

Journal

Neurochemistry InternationalElsevier

Published: Mar 1, 1996

References

  • Relations between slow extracellular potential changes, glial potassium buffering, and electrolyte and cellular volume changes during neuronal hyperactivity
    Dietzel, L.; Heinemann, U.; Lux, H.D.
  • Neuroglial localization of potassium and sodium effects on respiration in brain
    Hertz, L.
  • Effect of nerve impulses on the membrane potential of glial cells in the central nervous system of amphibia
    Orkand, R.K.; Nicholls, J.G.; Kuffler, S.W.
  • Subacute noradrenergic agonist infusions in vivo increase Na + , K + -ATPase and ouabain binding in rat cerebral cortex
    Swann, A.C.; Steketee, J.D.
  • Ouabain-sensitive and ouabain-resistant net uptake of potassium into astrocytes and neurons in primary cultures
    Walz, W.; Hertz, L.

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