EXTRACELLULAR N-ACETYLASPARTATE IN THE RAT-BRAIN - IN-VIVO DETERMINATION OF BASAL LEVELS AND CHANGES EVOKED BY HIGH K+

The purpose of this study was to determine the extracellular concentra tions of N-acetylaspartate (NAA) in the rat cerebral cortex, striatum, and hippocampus of halothane-anaesthetised rats by intracerebral micr odialysis, and to examine the effects of high K+-induced local depolar isation, which provokes synchronous neurotransmitter release, cell swe lling, and acid-base changes. Basal levels of NAA in the extracellular fluid (ECF) were determined by the zero net flux method. Tissue level s of NAA in the cortex, striatum, and hippocampus were 8.4, 5.7, and 7 .2 mmol/kg, respectively. The corresponding extracellular concentratio ns of NAA were much lower (35.1, 83.7, and 23.0 mu M). High tissue/ECF concentration ratios may suggest little release or leakage of NAA und er basal conditions, and potent reuptake mechanisms for NAA in the cel lular membrane of CNS cells. There was no change in ECF NAA during K+- induced local depolarising stimuli produced in the striatum, but NAA l evels consistently increased after the K+ stimuli, irrespective of whe ther or not Ca2+ was present in the perfusion medium. These data confi rm that NAA is not a neurotransmitter and suggest strongly that NAA is not directly involved in the release and reuptake or metabolism of ne uroactive compounds. The increase of NAA in the ECF immediately after K+ stimulation may reflect an involvement in brain osmoregulation and/ or acid-base homeostasis.