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Quantitative 13 C NMR studies of metabolic compartmentation in the adult mammalian brain
Author(s) -
Cruz Fátima,
Cerdán Sebastián
Publication year - 1999
Publication title -
nmr in biomedicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.278
H-Index - 114
eISSN - 1099-1492
pISSN - 0952-3480
DOI - 10.1002/(sici)1099-1492(199911)12:7<451::aid-nbm571>3.0.co;2-e
Subject(s) - glutamine , glutamate receptor , citric acid cycle , tricarboxylic acid , compartment (ship) , metabolism , flux (metallurgy) , biochemistry , glutamic acid , chemistry , biology , amino acid , biophysics , oceanography , receptor , organic chemistry , geology
We review the information obtained by 13 C NMR methods on the metabolic compartmentation of the adult mammalian brain with emphasis on its quantitative aspects. Classical radiotracer evidence and more recent 13 C NMR results support the presence in the brain of at least two glutamate pools, small and large , associated with two kinetically different tricarboxylic acid cycles localized in glia and neurons, respectively. Neuronal and glial cycles interact closely, utilizing common substrates like glucose and oxygen and exchanging a variety of metabolites including glutamate, glutamine and GABA. A model for the cerebral metabolism of (1,2− 13 C 2 ) acetate has made it possible to calculate fluxes through both cycles and evaluate the exchanges of glutamate, glutamine and GABA under different physiopathological conditions. Calculated flux values through the neuronal and glial tricarboxylic acid cycles are 1.0 and 0.4 µmol/min g, respectively. In the adult normoxic brain, the small and large glutamate pools account for approximately 10% and 90% of cerebral glutamate with estimated turnover times of 1.25 and 5.8/min, respectively. Net transfers of neuronal glutamate and GABA to the glial compartment are calculated to be 0.1 and 0.04 µmol/min g while transfer of glial glutamine to the neuronal compartment is estimated as 0.1 µmol/min g. Pyruvate recycling in the adult brain occurs mainly in the synaptic terminals with a calculated flux of 0.3 µmol/min g. These flux values are altered severely in pathological states such as hypothyroidism or ischemia. Copyright © 1999 John Wiley & Sons, Ltd.

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