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In vitro studies on the putative function of N-acetylaspartate as an osmoregulator.

Journal article
Authors Mattias Tranberg
Abdul-Karim Abbas
Mats Sandberg
Published in Neurochemical research
Volume 32
Issue 7
Pages 1248-55
ISSN 0364-3190
Publication year 2007
Published at Institute of Neuroscience and Physiology, Department of Physiology
Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology
Pages 1248-55
Language en
Links dx.doi.org/10.1007/s11064-007-9300-...
Keywords Animals, Aspartic Acid, analogs & derivatives, metabolism, Excitatory Amino Acid Agonists, metabolism, Hippocampus, cytology, metabolism, N-Methylaspartate, metabolism, Osmolar Concentration, Potassium, metabolism, Rats, Rats, Sprague-Dawley, Taurine, metabolism, Tissue Culture Techniques, Water-Electrolyte Balance
Subject categories Medical and Health Sciences

Abstract

Efflux and tissue content of N-acetylaspartate (NAA) and amino acids were evaluated from cultured and acutely prepared hippocampal slices in response to changes in osmolarity. The osmoregulator taurine, but not NAA, was lost from both types of slices after moderate reductions in extracellular osmolarity (-60 mOsm) for 10-48 h. Hypoosmotic shock (-166 mOsm) for 5 min resulted in unselective efflux of several amino acids from acutely prepared slices. Notably, the efflux of taurine, but not NAA, was prominent also after the shock. Efflux of NAA was markedly enhanced by NMDA and high K(+), in particular after the stimulation period. The high K(+)-mediated efflux was decreased by high extracellular osmolarity and a NMDA-receptor antagonist. The results indicate that NAA efflux can be induced by a sudden non-physiological decrease in extracellular osmolarity but not by prolonged more moderate changes in osmolarity. The mechanisms behind the efflux of NAA by high K(+) are complex and may involve both swelling and activation of NMDA-receptors.

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