Oligodendrocytes Do Not Export NAA-Derived Aspartate In Vitro.

摘要: Oligodendroglial cells are known to de-acetylate the N-acetylaspartate (NAA) synthesized and released by neurons use it for lipid synthesis. However, role of NAA regarding their intermediary metabolism remains poorly understood. Two hypotheses were proposed fate aspartate after being de-acetylation: (1) is metabolized in mitochondria oligodendrocyte lineage cells; (2) medium. We report here that aspartoacylase mRNA expression increases when primary rat progenitor (OPCs) differentiate into mature culture. Moreover, characterising metabolic functions acetyl coenzyme A from catabolism cultures 5 days using isotope-labelled glucose 5-days differentiation we found evidence extensive metabolism. Incubation with [1,6-13C]glucose followed gas chromatography–mass spectrometry high performance liquid chromatography analyses cell extracts media presence absence established acetate moiety produced hydrolysis does not enter mitochondrial form A. also resolved controversy concerning possible release medium: medium oligodendrocytes amounts detectable our methods. Therefore propose that: joins cytosolic pool rapidly takes part malate–aspartate shuttle, which transports reducing equivalents glycolysis ATP production enters tricarboxylic acid cycle at a slow rate.