TY - JOUR
T1 - Brain intermediary metabolism in vivo
T2 - Changes with carbon dioxide, development, and seizures
AU - Miller, Alexander L.
N1 - Funding Information:
Partially supported by U.S. Public Health Service grants MH 30511 (NIMH) and HD 09519 (NICHHD) and by a grant from the National Science Foundation (BNS 78-05161). ' Present address: Department of Psychiatry, The University of Texas Health Science Center, San Antonio, Texas.
PY - 1981/1/1
Y1 - 1981/1/1
N2 - This chapter reviews selected aspects of brain intermediary metabolism in vivo, with a focus on the recent developments in methodology and on changes found during development, seizures, and respiratory acidosis. The chapter discusses that carbon dioxide (CO2) levels play an important role in normal functioning of the central nervous system (CNS). Increased neuronal activity requires additional energy from oxidative phosphorylation, which raises the CO2 level in the milieu of the active neurons. This increased CO2 could then function to regulate local metabolism in two ways,(1) by causing an increase in local cerebral blood flow, it increases the flow of oxygen and glucose towards, and the movement of CO2 away from the active neurons, and (2) by inhibiting glycolysis, it slows the rate of development of an intracellular lactic acidosis, which may occur in response to a temporary imbalance between the rate of glycolysis and that of pyruvate oxidation. Metabolic consequences of the carbon dioxide treatment have important implications for investigators studying the effects of a variety of CNS depressants on energy metabolism.
AB - This chapter reviews selected aspects of brain intermediary metabolism in vivo, with a focus on the recent developments in methodology and on changes found during development, seizures, and respiratory acidosis. The chapter discusses that carbon dioxide (CO2) levels play an important role in normal functioning of the central nervous system (CNS). Increased neuronal activity requires additional energy from oxidative phosphorylation, which raises the CO2 level in the milieu of the active neurons. This increased CO2 could then function to regulate local metabolism in two ways,(1) by causing an increase in local cerebral blood flow, it increases the flow of oxygen and glucose towards, and the movement of CO2 away from the active neurons, and (2) by inhibiting glycolysis, it slows the rate of development of an intracellular lactic acidosis, which may occur in response to a temporary imbalance between the rate of glycolysis and that of pyruvate oxidation. Metabolic consequences of the carbon dioxide treatment have important implications for investigators studying the effects of a variety of CNS depressants on energy metabolism.
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U2 - 10.1016/S0074-7742(08)60290-1
DO - 10.1016/S0074-7742(08)60290-1
M3 - Article
C2 - 6792103
AN - SCOPUS:0019347376
SN - 0074-7742
VL - 22
SP - 47
EP - 82
JO - International Review of Neurobiology
JF - International Review of Neurobiology
IS - C
ER -