Histochemical and Biochemical Investigations on ATPase Activity Following Transient Brain Ischemia in Gerbils

  • Branka J. Mršulja
  • B. B. Mršulja


Cerebral ischemia is a serious complication of many disease processes which involves a various number of structural and biochemical changes, including edema. The pathophysiology of edema associated with a cerebrovascular lesion and its developmental patterns are sufficiently specific to warrant a separate classification of ischemic brain injury (16). Since ion concentration gradients across cell membranes are maintained by an energy-dependent pump mechanism (15, 33), it was assumed for a long time that fluid accumulation was an expression of a disturbed cellular osmoregulation arising from an “acute energy crisis” which develops during ischemia (7). However, we have not found any relationship between the early post-ischemic brain edema and cerebral energy metabolism: in post-ischemic brain edema and cerebral energy metabolism: in post-ischemia ATP and energy charge are restored within minutes but brain edema progresses (26). Concurrent with the increase in water content, the Na-K-ATPase activity progressively decreased, and as the water content declined, the enzyme activity was restored (26). Therefore, it was tentatively concluded that, among the many factors which are involved in the development and/or persistence of post-ischemic brain edema, the functioning of the Na-K-ATPase is of the utmost importance.


ATPase Activity Brain Edema Biochemical Investigation Adenosine Triphosphatase Neuronal Perikaryon 
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.
    Borgers, M. (1973): The cytochemical application of new potenti inhibitors of alkaline phosphatases. J. Histochem. Cytochem. 21: 812–824.Google Scholar
  2. 2.
    Brightman, M.W., Anders, J.J., Schmechel, D., and. Rosenstein, J.M. (1978): The lability of the shape and content of glial cells. In: Dinamic properties of glia cells. Eds: E. Schoffeniels, G. Franck, L. Hertz, and D.B. Tower, Pergamon Press, Oxford, New York, pp. 21–44.Google Scholar
  3. 3.
    Djuricic, B.M., and Mxsulja, B.B. (1977): Enzymic activity of the brain: microvessels vs. total forebrain homogenate. Brain Res. 138: 561–564.PubMedCrossRefGoogle Scholar
  4. 4.
    Ernst, S.A. (1972): Transport adenosine triphosphatase cytochemistry: II. Cytochemical localization of ouabain-sensitive, potassium dependent phosphatase activity in the secretory epithelium of the avian salt gland. J. Histochem. Cytochem. 20: 23–38.Google Scholar
  5. 5.
    Ernst, S.A. (1973): Cytochemical localization of phosphatase activity in rat kidney cortex. J. Cell Biol. 59: (2, Pt. 2 ) 93a (abstr.)Google Scholar
  6. 6.
    Friede, R.L. (1965): Enzyme histochemistry of neuroglia. In: Biology of Neuroglia,Progress in Brain Res., Vol. 15, Eds. E.D.P. de Robertis and R. Carrea, Elsevier Publishing Company., Amsterdam, London, New York, pp. 35–47.CrossRefGoogle Scholar
  7. 7.
    Fujimoto, T., Walker, J.T., Jr., Spatz, M., and Klatzo, I. (1976): Pathophysiologic aspects of ischemic edema. In: Dynamics of Brain Edema, eds. H.M. Pappius and W. Feindel, Springer Verlag, New York, pp. 171–180.CrossRefGoogle Scholar
  8. 8.
    Garcia, J.H., Lossinsky, A.S., Nishimoto, K., Klatzo, I., and Lightfoote, W. Jr. (1978): Cerebral mic- rovasculature in ischemia. In: Pathology of Cerebrispinal Microcirculation Advance in Neurology, Vol. 20, Fds. J. Cervos-Navarro, E. Betz, G. Fbhardt, R. Ferszt and R. Wullenweber, Raven Press, New York, pp. 141–149.Google Scholar
  9. 9.
    Guth, L., and Albers R.W. (1974): Histochemical demonstration of (Na - K+)-activated adenosine triphosphatase. J. Histochem. Cytochem. 22: 320326.Google Scholar
  10. 10.
    Hamberger, A., Blomstrand, C., and Lehninger, A.L. (1970): Comparative studies on mitochondria isolated from neuron-enriched and glia-enriched fractions of rabbit and beef brain. J. Cell Biol. 45: 221–229.PubMedCrossRefGoogle Scholar
  11. 11.
    Hess, H.H., Embree, L.J., and Shein, H.M. (1972): Enzyme control of. Na-and K- active transport in normal and neoplastic rodent astroglia. Prog. Exp. Tumor Res. 17: 308–315.Google Scholar
  12. 12.
    Huttenlocher, P.R., and Rawson, M.D. (1968): Neuronal activity and adenosine triphosphatase in immature cerebral cortex. Exp. Neurol. 22: 118–129.Google Scholar
  13. 13.
    Katz, A.I., and Epstein, F.H. (1967): Role of sodium potassium-activated adenosine triphosphatase in absorption of sodium in kidney. J. Clin. Invest. 46: 1999–2011.Google Scholar
  14. 14.
    Katzman, R., Alen, F., and Wilson, C. (1963): Further observations on triethyltin edema. Archs Neurol. ( Paris ) 9: 178–187.Google Scholar
  15. 15.
    Katzman, R., and Pappius, H.M. (1973): Brain electrolytes and fluid metabolism. Williams and Wilkins, Baltimore.Google Scholar
  16. 16.
    Klatzo, I. (1975): Pathophysiologic aspects of cerebral ischemia. In: The Nervous System, edited by D.B. Tower, Vol. 1, Raven Press, New York, pp. 313–322.Google Scholar
  17. 17.
    Klatzo, I. (1979): Cerebral edema and ischemia. In: Recent Advances in Neuropathology, Fds. W.T. Smith and J.B. Cavanagh, Vol. 1, Churchill Livinstone, Edinburgh-London-TTew York, pp. 27–39.Google Scholar
  18. 18.
    Kometiani, P., Kometiani, Z., and Mikeladze, D. (1978): 3’,5’-AMP-dependent protein kinase ana. membrane ATPase of the nerve cell. Progress in Neurobiology 11: 223–247.Google Scholar
  19. 19.
    Lewin, E., and Hes, H_H. (1964): Intralaminar distribution of Na, K -ATPase in rat cortex. J. Neurochem. 11: 473–482.Google Scholar
  20. 20.
    Lewin, E., and McCrimmon, A. (1967): ATPase activity of discharging cirtical lesions induced by freezing. Archs Neurol. 16: 321–325.CrossRefGoogle Scholar
  21. 21.
    Lowry, O.H., and Passonneau, J.V. (1972): A Flexible System of Enzymatic Analyses. Academic Press, New York.Google Scholar
  22. 22.
    Lowry, O.H., Rosenbrough, N.J., Farr, A.L., and Randall, J.R. (1951): Protein measurements with the Folin phenol reagent. J. Biol. Chem. 193: 265–275.Google Scholar
  23. 23.
    Medzihradsky, F., Sellinger, O.Z. Nandhasri, P.S., and Santiago, J.C. (1972): ATPase activity in glial cells an’s in neuronal perikarya of rat cerebral cortex during early postnatal development. J. Neurochem. 19: 543–545.PubMedCrossRefGoogle Scholar
  24. 24.
    Medzihradsky, F., Sellinger, O.Z., Nandhasri, P.S., and Santiago, J.C. (1974): Adenosine triphosphatase activity in glial cells and in neuronal perikarya of edematous rat brain. 67: 133–139.Google Scholar
  25. 25.
    Mrsulja, B.B., Mrsulja, B.J., Cvejic, V., Djuricic, B.M., and Rogac, LJ. (1978): Alterations of putative neurotransmitters and enzymes during ischemia in gerbil cerebral cortex. J. Neural. Transm., Suppl. 14: 23–30.Google Scholar
  26. 26.
    Mrsulja, B.B., Djuricic, B.M., Cvejic, V., Mrsulja, B.J., Abe, T., Spatz, M. and Klatzo, I. (1979): Biochemistry of experimental ischemic brain edema. Proc. of the First Intern. Ernst Reuter Symposium, Brain Edema, Berlin (In press), Raven Press, New York.Google Scholar
  27. 27.
    Mrsulja, B.J., Spatz, M. and Klatzo, I. (1979): Cytóchemistry of Hippocampus following cerebral ischemia. In: Pathophysiology of Cerebral Energy Metabolism, Eds. B.B. Mrsulja. Lj., M. Rakic, I. Klatzo and M. Spatz, Plenum Press, New York, London, pp. 73–90.Google Scholar
  28. 28.
    Mrsulja, B.J., Spatz, M., ‘Talker, J.T., Jr., and Klatzo, I. (1979): Histochemical investigation of the Mongolian Gerbil’s brain during unilateral ischemia. Acta Neuropathol. ( Berl. ) 46: 123–131.Google Scholar
  29. 29.
    Nishimoto, K., Wolman, M., Spatz, M. and Klatzo, I. (1978): Pathophysiologic correlations in the blood brain barrier damage due to air embolism. In: Pathology of Cerebral Microcirculation-Advances in Neurology, Vol. 20, Eds. J. Cervos-Navarro, E. Betz, G. Fbhardt, R. Ferszt, R. Nullenweber, Raven Press, New York, pp. 237–244.Google Scholar
  30. 30.
    Ostenda, M., Szumanska, G., and Gadamski, R. (1978): Specific hydrolases activity in blood vessels of rabbit brain after circulatory hypoxia. In: Pathophysiological, Biochemical and Morphological Aspects of Cerebral Ischemia and Arterial Hypertension. Eds. M.J. Mossakowski, I.B. Zelman, and H. Kroh, Warsaw, pp. 60–66.Google Scholar
  31. 31.
    Rigoulet, M., Guerin, B., Cohadon, F., and Vandendreissche, M. (1979): Unilateral brain injury in the rabbit; reversible and irreversible damage of the membranal ATPases. J. Neurochem. 32: 535–541.PubMedCrossRefGoogle Scholar
  32. 32.
    Scrimgeour, K.G. (1977): Chemistry and control of enzyme reactions. Academic Press, London.Google Scholar
  33. 33.
    Skou, J.C. (1915): Enzymatic basis for active transport of Na and K across cell membrane. Physiol. Rev. 45: 596–617.Google Scholar
  34. 34.
    Somjen, G.G., Rosenthal, M., Cordingley, G., Lamanna, J., and Lothman, E. (1976): Potassium, neuroglia, and oxidative metaboliam in central gray matter. Fed. Proc. 35: 1266–1271.Google Scholar
  35. 35.
    Stahl, W.L.,+anq Broderson, S.H. (1976): Localization of Na K -ATPase in brain. Fed. Proc. 35: 1260–1265.Google Scholar
  36. 36.
    Stahl, W.L., Spence, A.M., Coates, P.W., and Broderson, S.H. (1978.: Studies on cellular localization on Na, K -ATPase activity in nervous tissue. In: Dynamic Properties of Glia Cells. Fds. E. Schoffeniels, G. Franck, L. Hertz, D.B. Tower, Pergamon Press, Oxford, New York, pp. 371–381.Google Scholar

Copyright information

© Plenum Press, New York 1980

Authors and Affiliations

  • Branka J. Mršulja
    • 1
    • 2
  • B. B. Mršulja
    • 1
    • 2
  1. 1.Division of Neurophysiology and NeurochemistryInstitute for Biological ResearchBelgradeYugoslavia
  2. 2.Laboratory of Neurochemistry, Faculty of MedicineInstitute of BiochemistryBelgradeYugoslavia

Personalised recommendations