By Robert C. Vannucci, Fred Plum (auth.), Gerald E. Gaull (eds.)
The development of neurochemistry. molecular biology, and biochemical genetics has ended in a burgeoning of latest info proper to the pathogenesis of mind disorder. This explosion of fascinating new details is crying out for collation and significant synthesis. In its totality, it defies systematic summa tion, and, after all, nobody writer can cope. hence invites for contributions got to numerous specialists in parts that are lower than energetic research, of present neurological curiosity, and pregnant. even if this undertaking is comparatively entire, by means of dint of dimension. different themes could have been incorporated; the choice used to be exclusively my accountability. i feel systematic summation a digital impossibility-indeed, rarely definitely worth the attempt. The try to gather the entire sections concerned about a wide treatise with a number of authors necessarily leads to untoward delays because of the distinction within the price at which a variety of authors paintings. accordingly, the next procedure has been followed: a number of small volumes and a comparatively versatile layout, with ebook so as of receipt and once sufficient chapters are assembled to make ebook functional and affordable. during this means, the time lag among the tips and their emergence in print is the shortest.
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Additional resources for Biology of Brain Dysfunction: Volume 3
Bioi. Chem. 241:3997-4003 (1966). 97. O. H. Lowry, J. V. Passonneau, F. X. Hasselberger, and D. W. Schulz, Effect of ischemia on Perinatal Hypoxic-Ischemic Brain Damage 98. 99. 100. 101. 102. 103. 104. 105. 106. 107. 108. 109. 110. Ill. 112. 113. 114. 115. 116. 117. 118. 119. 120. 121. 122. 41 known substrates and cofactors of the glycolytic pathway in brain, J. Bioi. Chem. 239:18-30 (1964). H. S. Bachelard, in "Handbook of Neurochemistry" (A. ) Vol. 4, pp. I-II, Plenum Press, New York (1970).
These products of fatty acid catabolism enter the brain and are oxidatively metabolized via the TeA cycle to yield energy. (128,129) However, under conditions of hypoxia and anoxia, the consumption of ketone bodies in brain should be reduced or cease altogether, since their utilization to form energy requires the presence of oxygen. Amino acids also can be catabolized only via oxidative metabolism. Additional evidence that ketone bodies and amino acids are of little importance during hypoxia stems from the observation that fetal animals, who exhibit the greatest anoxic resistance, appear to use glucose as the predominant or sole cerebral fuel.
During recovery brain pyruvate increases, accompanied by a slight decline in lactate and a rise in glucose. These shifts indicate that during reoxygenation lactate is actively oxidized to pyruvate at a time when glucose consumption is still minimal. For as much as an hour of recovery, lactate remains the preferred substrate for oxidative metabolism via the TeA cycle, and as a result brain glucose concentrations rise above control levels. 16 12 Lactate 8 4 ~ '" '0 E E 0 6 4 2 o ~~--~~~--~--------~~~--~ Min 0 10 ANOXIA 30 50 RECOVERY 80 140 Fig.