Cholinergic Systems and Disorders of Carbohydrate Catabolism

  • J. P. Blass
  • G. E. Gibson
Part of the Advances in Behavioral Biology book series (ABBI, volume 24)


During the last 5 years a number of observations have come together to indicate that cholinergic functions are particularly sensitive to hypoxia or other conditions which impair carbohydrate oxidation by the brain. The evidence includes biochemical studies in vitro and in vivo, electrophysiological studies, and clinical observations, and includes work done in a number of laboratories. In discussing these findings and their clinical implications, it is crucial to distinguish between conditions in which the oxidation of substrate by the brain is totally abolished and conditions in which it is more or less impaired but not abolished. In the former, exemplified by total anoxia, the homeostatic mechanisms of the brain fail; levels of ATP and other high energy compounds fall within seconds, and autolysis and death follow soon (5, 24, 25). In contrast, in graded mild hypoxia, the homeostatic mechanisms of the brain appear to be reset so as to maintain the levels of high energy compounds by reducing their utilization. At least 6 laboratories, including our own, have now shown that hypoxia can severely impair neurological function without reducing levels of ATP in the brain (10–13, 26, 31, 34, 35, 37, 42). This point has been documented in great detail by Siesjo’s group in Lund (26, 31, 34, 35; Table 1).


Methylmalonic Acid Carbohydrate Oxidation Cholinergic Function Mild Hypoxia Pyruvate Oxidation 
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Copyright information

© Plenum Press, New York 1978

Authors and Affiliations

  • J. P. Blass
    • 1
  • G. E. Gibson
    • 1
  1. 1.Departments of Psychiatry and Biological Chemistry, School of Medicine, and the Mental Retardation Research CenterUniversity of CaliforniaLos AngelesUSA

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