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- Title
Kinetics of glial glutamine efflux and the mechanism of neuronal uptake studied in vivo in mildly hyperammonemic rat brain.
- Authors
Kanamori, Keiko; Ross, Brian D.
- Abstract
Kinetics of glial glutamine (GLN) transport to the extracellular fluid (ECF) and the mechanism of GLNECF transport into the neuron – crucial pathways in the glutamine–glutamate cycle – were studied in vivo in mildly hyperammonemic rat brain, by NMR and microdialysis to monitor intra- and extracellular GLN. The minimum rate of glial GLN efflux, determined from the rate of GLNECF increase during perfusion of α-(methylamino)isobutyrate (MeAIB), which inhibits neuronal GLNECF uptake by sodium-coupled amino-acid transporter (SAT), was 2.88 ± 0.22 μmol/g/h at steady-state brain [GLN] of 8.5 ± 0.8 μmol/g. Our previous study showed that the rate of glutamine synthesis under identical experimental conditions was 3.3 ± 0.3 μmol/g/h. At steady-state glial [GLN], this is equal to its efflux rate to the ECF. Comparison of the two rates suggests that SAT mediates at least 87 ± 8% (= 2.88/3.3 × 100%) of neuronal GLNECF uptake. While MeAIB induced > 2-fold elevation of GLNECF, no sustained elevation was observed during perfusion of the selective inhibitor of LAT, 2-amino-bicyclo[1,1,2]heptane-2-carboxylic acid (BCH), or ofd-threonine, a putative selective inhibitor of ASCT2-mediated GLN uptake. The results strongly suggest that SAT is the predominant mediator of neuronal GLNECF uptake in adult rat brain in vivo.
- Subjects
PHYSIOLOGICAL effects of glutamine; MICRODIALYSIS; EXTRACELLULAR fluid; METHYLAMINES; AMINO acid neurotransmitters
- Publication
Journal of Neurochemistry, 2006, Vol 99, Issue 4, p1103
- ISSN
0022-3042
- Publication type
Article
- DOI
10.1111/j.1471-4159.2006.04152.x