Neuroprotection Methods and Protocols pp 79-98

Part of the Methods in Molecular Biology book series (MIMB, volume 399)

Biochemical Methods to Assess the Coupling of Brain Energy Metabolism in Control and Disease States

  • Jennifer Zechel
  • W. David Lust
  • Michele Puchowicz

Abstract

Mitochondrial dysfunction has been increasingly shown as a critical process that makes certain areas of the brain more susceptible not only to neurological disease but also to aging. Quantitative histochemistry is a series of procedures for measuring select metabolites in discrete regions of the brain, as they exist in vivo. The development of this method has been useful in establishing energy imbalance following ischemia but more recently has become useful in studying those processes related to the mitochondria which make the brain more susceptible to a variety of neurological insults. The relatively inexpensive cost to assay a given brain metabolite makes this methodology useful in the interpretation of molecular and biochemical responses in terms of the condition of the tissue following a neurological insult.

Key Words

Brain high-energy phosphates redox states pathologically induced-energy imbalance 

References

  1. 1.
    Greengard P (1956) Determination of intermediary metabolites by enzymic fluorimetry. Nature 178: 632–4.CrossRefGoogle Scholar
  2. 2.
    Lowry OH, Passonneau JV (1972) A Flexible System of Enzymatic Analysis. New York: Academic Press.Google Scholar
  3. 3.
    Lust WD, Feussner GK, Barbehenn EK, Passonneau JV (1981) The enzymatic measurement of adenine nucleotides and P-creatine in picomole amounts. Anal. Biochem. 110: 258–66.CrossRefGoogle Scholar
  4. 4.
    Lundin A, Richardsson A, Thore A (1976) Continuous monitoring of ATP-converting reactions by purified firefly luciferase. Anal. Biochem. 75: 611–20.CrossRefGoogle Scholar
  5. 5.
    Siesjo BK (1978) Brain energy metabolism and catecholaminergic activity in hypoxia, hypercapnia and ischemia. J. Neural Transm. Suppl. 17–22.Google Scholar
  6. 6.
    Lenox RH, Kant GH, Meyerhoff JL (1982) Rapid enzyme inactivation. In: Lajtha A, ed. Handbook of Neurochemistry. New York: Plenum, pp. 77–102.Google Scholar
  7. 7.
    Lust WD, Passonneau JV, Veech RL (1973) Cyclic adenosine monophosphate, metabolites, and phosphorylase in neural tissue: a comparison a methods of fixation. Science 181: 280–2.CrossRefGoogle Scholar
  8. 8.
    Lust WD, Murakami N, de Azeredo F, Passonneau JV (1980) A comparison of methods for brain fixation. In: Passonneau JV, Hawkins RA, Lust WD, Welsh RA, eds. Cerebral Metabolism and Neural Function. Baltimore: Williams and Wilkins, pp. 10-9.Google Scholar
  9. 9.
    Lust WD, Ricci AJ, Selman WR, Ratcheson RA (1989) Methods of fixation of nervous tissue for use in the study of cerebral energy metabolism. In: Boulton, AA; Baker, GB; Butterworth, RF, eds. Carbohydrates and Energy Metabolism. Totowa, NJ: Humana Press, pp. 1–42.CrossRefGoogle Scholar
  10. 10.
    Goldberg ND, Passonneau JV, Lowry OH (1966) Effects of changes in brain metabolism on the levels of citric acid cycle intermediates. J. Biol. Chem. 241: 3997–4003.Google Scholar
  11. 11.
    Ponten U, Ratcheson RA, Salford LG, Siesjo BK (1973) Optimal freezing conditions for cerebral metabolites in rats. J. Neurochem. 21: 1127–38.CrossRefGoogle Scholar
  12. 12.
    Mrsulja BB, Ueki Y, Lust WD (1986) Regional metabolite profiles in early stages of global ischemia in the gerbil. Metab. Brain Dis. 1: 205–20.CrossRefGoogle Scholar
  13. 13.
    Harik SI, al Mudallal AS, LaManna JC, Lust WD, Levin BE (1997) Ketogenic diet and the brain. Ann. N. Y. Acad. Sci. 835: 218–24.CrossRefGoogle Scholar

Copyright information

© Humana Press Inc. 2007

Authors and Affiliations

  • Jennifer Zechel
    • 1
  • W. David Lust
    • 1
  • Michele Puchowicz
    • 2
  1. 1.Department of Experimental Neurological SurgeryCase Western Reserve University School of MedicineCleveland
  2. 2.Department of AnatomyCase Western Reserve University School of MedicineCleveland

Personalised recommendations