Acetylcholine Synthesis and Glucose Oxidation with Various Oxygen Levels invivo and invitro

  • G. E. Gibson
  • H. J. Ksiezak
  • T. E. Duffy
Part of the Advances in Behavioral Biology book series (ABBI, volume 25)


Normal brain function is dependent upon a continual supply of oxygen. For example, memory and the ability to learn a complex task are impaired when the arterial oxygen tension (PaO2) is reduced from a normal of approximately 90 mm Hg to about 60 mm Hg (13). The biochemical basis of the brain’s sensitivity to a decrease in oxygen (hypoxic hypoxia) is unknown, but it is apparently not due to an inability to maintain the level of energy metabolites (5,14). Consequently, the focus in the search for the molecular mechanism in hypoxia has shifted to those neurotransmitters whose synthesis depends upon oxygen. The rate-limiting step in the formation of dopamine, norepinephrine and serotonin requires molecular oxygen; furthermore, their turnover is decreased by hypoxia. However, the importance of decreased catecholamine and serotonin synthesis in the development of symptoms of hypoxia remains questionable since the turnover of these neurotransmitters is not reduced when hypoxia is accompanied by stress (2).


Glucose Oxidation Citric Acid Cycle Arterial Oxygen Tension 14C02 Production Normal Brain Function 
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  1. 1.
    Booth, R.F.G. and Clark, J.B. (1978): Biochem. J. 176:365–370.Google Scholar
  2. 2.
    Davis, J.N., Giron, L.T., Stanton, E. and Maury, W. (1979): Adv. Neurol. 26:219–223.Google Scholar
  3. 3.
    Dolivo, M. (1974): Fed. Proc. Amer. Soc. Exp. Biol. 33:1043–1048.Google Scholar
  4. 4.
    Drachman, D.A. (1978): IN Psychopharmacology: A Generation of Progress (eds) M.A. Lipton, A. DiMascio and K.F. Killam, Raven Press, New York, pp. 651–662.Google Scholar
  5. 5.
    Duffy, T.E., Nelson, S.R. and Lowry, O.H. (1972): J. Neurochem. 19:.959–977.CrossRefGoogle Scholar
  6. 6.
    Freeman, J.J., Choi, R. and Jenden, D.J. (1975): J. Neurochem. 24:729–734.Google Scholar
  7. 7.
    Gibson, G.E. and Blass, J.P. (1976): J. Neurochem. 27:37–42.CrossRefGoogle Scholar
  8. 8.
    Gibson, G.E. and Blass, J.P. (1976): J. Neurochem. 26:1073–1078.CrossRefGoogle Scholar
  9. 9.
    Gibson, G.E. and Blass, J.P. (1979): Biochem. Pharmacol. 28: 133–140.CrossRefGoogle Scholar
  10. 10.
    Gibson, G.E. and Shimada, M. (1980): Biochem. Pharmacol. 29:167–174.CrossRefGoogle Scholar
  11. 11.
    Gibson, G.E., Shimada, M. and Blass, J.P. (1978): J. Neurochem. 31:757–760.CrossRefGoogle Scholar
  12. 12.
    Harkonen, M.H.A., Passonneau, J.V. and Lowry, O.H. (1969): J. Neurochem. 16:1439–1450.CrossRefGoogle Scholar
  13. 13.
    Luft, U.C. (1975): IN Handbook of Physiology, Sect. 3: Respiration (eds) W.O. Fenn and H. Rahn, American Physiological Society, Washington, pp. 1099–1145.Google Scholar
  14. 14.
    Siesjo, B.K. and Nilsson, L. (1971): Scand. J. Clin. Lab. Invest. 27:83–96CrossRefGoogle Scholar

Copyright information

© Plenum Press, New York 1981

Authors and Affiliations

  • G. E. Gibson
    • 1
  • H. J. Ksiezak
    • 1
  • T. E. Duffy
    • 1
  1. 1.Department of NeurologyCornell Medical College, and The Burke Rehabilitation CenterWhite PlainsUSA

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