Quantification of cortical GABA-glutamine cycling rate using in vivo magnetic resonance signal of [2-13C]GABA derived from glia-specific substrate [2-13C]acetate

Neurochem Int. 2007 Jan;50(2):371-8. doi: 10.1016/j.neuint.2006.09.011. Epub 2006 Oct 23.

Abstract

Brain [2-(13)C]gamma-aminobutyric acid (GABA) signal derived from the glia-specific substrate [2-(13)C]acetate reflects the extent of the GABA-glutamine neurotransmitter cycling between GABAergic neurons and glial cells. We report, for the first time, in vivo quantification of the GABA-glutamine cycling flux. The GABA-glutamine cycling flux rate was determined to be 1.8+/-0.4 micromol/(gh) (mean+/-S.D., n=6, approximately 6% of total tricarboxylic acid cycle rate) in the neocortex of vigabatrin-treated rats. The relatively small magnitude of glial contribution to the clearance of extracellular GABA measured in this study provided in vivo evidence to support the concept of a significant neuronal reuptake of GABA, which short-circuits the GABA-glutamine cycling pathway for repletion of released neurotransmitter GABA.

Publication types

  • Research Support, N.I.H., Intramural

MeSH terms

  • Acetates / metabolism
  • Animals
  • Cerebral Cortex / cytology
  • Cerebral Cortex / metabolism*
  • Cyclohexanecarboxylic Acids / pharmacology
  • Enzyme Inhibitors / pharmacology
  • Female
  • Glucose / metabolism
  • Glutamine / metabolism*
  • Kinetics
  • Macaca mulatta
  • Magnetic Resonance Spectroscopy
  • Male
  • Neuroglia / metabolism*
  • Rats
  • Rats, Sprague-Dawley
  • Vigabatrin / pharmacology
  • gamma-Aminobutyric Acid / metabolism*

Substances

  • Acetates
  • Cyclohexanecarboxylic Acids
  • Enzyme Inhibitors
  • Glutamine
  • gabaculine
  • gamma-Aminobutyric Acid
  • Vigabatrin
  • Glucose