1. Norwegian Defence Research Establishment, Division for Environmental Toxicology, Kjeller, Norway
2. ^*M.R. Centre, Department of Physics, University of Nottingham, Nottingham, United Kingdom
3. ^†MR Center, SINTEF-UNIMED, Trondheim, Norway

Correspondence: Bjornar Hassel, Norwegian Defence Research Establishment, Division for Environmental Toxicology, P.O.B. 25, N-2007 Kjeller, Norway.

Received 21 August 1996; Revised 12 June 1997; Accepted 21 July 1997.

Abstract

Glial-neuronal interchange of amino acids was studied by ¹³C nuclear magnetic resonance spectroscopy of brain extracts from fluoroacetate-treated mice that received [1,2-¹³C]acetate and [1-¹³C]glucose simultaneously. [¹³C]Acetate was found to be a specific marker for glial metabolism even with the large doses necessary for nuclear magnetic resonance spectroscopy. Fluoroacetate, 100 mg/kg, blocked the glial, but not the neuronal tricarboxylic acid cycles as seen from the ¹³C labeling of glutamine, glutamate, and -aminobutyric acid. Glutamine, but not citrate, was the only glial metabolite that could account for the transfer of ¹³C from glia to neurons. Massive glial uptake of transmitter glutamate was indicated by the labeling of glutamine from [1-¹³C]glucose in fluoroacetate-treated mice. The C-3/C-4 enrichment ratio, which indicates the degree of cycling of label, was higher in glutamine than in glutamate in the presence of fluoroacetate, suggesting that transmitter glutamate (which was converted to glutamine after release) is associated with a tricarboxylic acid cycle that turns more rapidly than the overall cerebral tricarboxylic acid cycle.