Calcium Movements in Brain During Failure of Energy Metabolism

  • E. Zhang
  • M. Lauritzen
  • T. Wieloch
  • A. J. Hansen


The interstitial ion concentrations in brain are maintained within narrow limits. Changes in plasma concentrations are effectively dealt with by the low ionic permeability of the blood-brain barrier combined with active transport processes located in the brain endothelium and in the choroid plexus [3]. The most important reason for disturbances in brain ion milieu is the fact that the ions are not in electrochemical equilibrium across the cell membrane. Active transport processes are constantly needed to counteract the passive dissipation of the ion gradients.


Severe Hypoglycemia Cortical Spreading Depression Spreading Depression Cereb Blood Flow Brain Energy Metabolism 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. 1.
    Benveniste H, Drejer J, Schousboe A, Diemer NH (1984) Elevation of the extracellular concentrations of glutamate and aspartate in rat hippocampus during transient cerebral ischemia monitored by intracerebral microdialysis. J Neurochem 43:1369–1374PubMedCrossRefGoogle Scholar
  2. 2.
    Biscoe TJ, Duchen MR, Eisner DA, O’Neill SC, Valdeolmillos M (1988) The effects of glucose removal and cyanide on intracellular Ca in isolated, single mouse dorsal root ganglion cells.Google Scholar
  3. 3.
    Bradbury MWB (1979) The concept of a blood-brain barrier. Wiley, Chichester,UKGoogle Scholar
  4. 4.
    Dietzel I, Heinemann U, Hofmeier G, Lux HD (1982) Stimulus-induced changes in extracellular Na and Cl concentration in relation to changes in the size of the extracellular space. Exp Brain Res 46:73–84PubMedCrossRefGoogle Scholar
  5. 5.
    DingledineR, Somjen G (1981) Calcium dependence of synaptic transmission in the hippocampal slice. Brain Res:218–222Google Scholar
  6. 6.
    Goroleva NA, Koroleva VI, Amemore T, Pavlik V, Bures J (1987) Ketamine blockade of cortical spreading depression in rats. Electroencephalogr Clin Neurophysiol 66:440–447CrossRefGoogle Scholar
  7. 7.
    Hansen AJ (1985) Effect of anoxia on ion distribution in the brain. Physiol Rev 65:101–148PubMedGoogle Scholar
  8. 8.
    Hansen AJ, Olsen C-E (1980) Brain extracellular space during spreading depression and ischemia. Acta Physiol Scand 108:355–365PubMedCrossRefGoogle Scholar
  9. 9.
    Hansen AJ, Zeuthen T (1980) Extracellular ion concentration during spreading depression and ischemia in the rat brain cortex. Acta Physiol Scand 113:437–445CrossRefGoogle Scholar
  10. 10.
    Hansen AJ, Lauritzen M, Wieloch T (1988) NMD A antagonists inhibit cortical spreading depression but not anoxie depolarization. In: Frontiers in excitatory amino acid research. Alan R Liss, New York (in press)Google Scholar
  11. 11.
    Harris RJ, Wieloch T, Symon L, Siesjo BK (1984) Cerebral extracellular calcium activity in severe hypoglycemia: relation to extracellular potassium and energy state. J Cereb Blood Flow Metab 4:187–193PubMedCrossRefGoogle Scholar
  12. 12.
    Heinemann U, Louvel J (1983) Changes in Ca+ + and K+ during repetitive electrical stimulation and during pentetrazol induced seizure activity in the sensorimotor cortex of cats. Pfluegers Arch 398:310–317CrossRefGoogle Scholar
  13. 13.
    Krivanek J (1961) Some metabolic changes accompanying Leao’s spreading cortical depression in the rat. J Neurochem 6:183–199PubMedCrossRefGoogle Scholar
  14. 14.
    Krnjević K, Leblond J, Morris ME (1988) Anoxia-evoked increases in extracellular Ca in isolated rat hippocampal slices. J Physiol 400:24PGoogle Scholar
  15. 15.
    Leão AAP (1944) Spreading depression of activity in cerebral cortex. J Neurophysiol 7:359–390Google Scholar
  16. 16.
    Lehmenkuhler A (1979) Interrelationships between DC-potentials, potassium activity, pO2 and pCO2 in the cerebral cortex of the rat. In: Speckmann E-J, Caspers H (eds) Origin of cerebral field potentials. Thieme, Stuttgart, pp 49–58Google Scholar
  17. 17.
    Mies G, Paschen W (1984) Regional changes of blood flow, glucose and ATP content determined on brain sections during a single passage of spreading depression in rat brain cortex. Exp Neurol 84:249–258PubMedCrossRefGoogle Scholar
  18. 18.
    Nedergaard M, Astrup J (1986) Infarct rim: effect of hyperglycemia on direct current potential and (14C)2-deoxyglucose phosphorylation. J Cereb Blood Flow Metab 6:607–615PubMedCrossRefGoogle Scholar
  19. 19.
    Nedergaard M, Hansen AJ (1988) Spreading depression is not associated with neuronal injury in the normal brain. Brain Res 449:395–398PubMedCrossRefGoogle Scholar
  20. 20.
    Norberg K, Siesjo BK (1976) Oxidative metabolism of the cerebral cortex of the rat in insulin-induced hypoglycemia. J Neurochem 26:345–352PubMedCrossRefGoogle Scholar
  21. 21.
    Novelli A, Reilly JA, Lysko PG, Henneberry RC (1988) Glutamate becomes neurotoxic via the N-ethyl-D-aspartate receptor when intracellular energy levels are reduced. Brain Res 451:205–212PubMedCrossRefGoogle Scholar
  22. 22.
    Pellegrino D, Almquist L-O, Siesjo BK (1981) Effects of insulin-induced hypoglycemia on intracellular pH and impedance in the cerebral cortex of the rat. Brain Res 221:129–147CrossRefGoogle Scholar
  23. 23.
    Quistdorff B, Gjedde A, Hansen AJ (1979) Spatial analysis of the freeze-trapped brain provides for temporal resolution of an event. Metabolic, electrical and blood flow changes during spreading depression. Acta Physiol Scand 105:42AGoogle Scholar
  24. 24.
    Sandberg M, Butcher SP, Hagberg H (1986) Extracellular overflow of neuroactive amino acids during severe insulin-induced hypoglycemia: in vivo dialysis of the rat hippocampus. J Neurochem 47:178–184PubMedCrossRefGoogle Scholar
  25. 25.
    Schanne FAX, Kane AB, Young EE, Faber JL (1979) Calcium dependence of toxic cell death: a final common pathway. Science 206:700–702PubMedCrossRefGoogle Scholar
  26. 26.
    Siemkowicz E, Hansen AJ (1981) Brain extracellular ion composition and EEG activity following 10 minutes ischemia in normo-and hyperglycemic rats. Stroke 12:236–240PubMedCrossRefGoogle Scholar
  27. 27.
    Siesjö BK (1978) Brain energy metabolism. New York, WileyGoogle Scholar
  28. 28.
    Siesjo BK (1981) Cell damage in the brain: a speculative synthesis. J Cereb Blood Flow Metab 1:155–185PubMedCrossRefGoogle Scholar
  29. 29.
    Simon RP, Swan JH, Griffiths T, Meldrum BS (1984) Blockade of N-methyl-D-aspartate receptors may protect against ischemic damage in the brain. Science 226:850–852PubMedCrossRefGoogle Scholar
  30. 30.
    Van Harreveld A, Fifkova E (1970) Glutamate release from the retina during spreading depression. J Neurobiol 2:13–29PubMedCrossRefGoogle Scholar
  31. 31.
    Wieloch T (1985) Hypoglycemia-induced neuronal damage prevented by an N-methyl-D-as-partate antagonist. Science 230:681–683PubMedCrossRefGoogle Scholar
  32. 32.
    Wieloch T, Harris RJ, Symon L, Siesjo BK (1984) Influence of severe hypoglycemia on brain extracellular calcium and potassium activities, energy, and phospholipid metabolism. J Neurochem 43:160–168PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 1989

Authors and Affiliations

  • E. Zhang
    • 1
  • M. Lauritzen
    • 1
  • T. Wieloch
    • 2
  • A. J. Hansen
    • 1
  1. 1.Department of General Physiology and BiophysicsUniversity of CopenhagenCopenhagen NDenmark
  2. 2.Laboratory of Experimental Brain ResearchUniversity of LundS-LundSweden

Personalised recommendations