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Searching for Mechanisms of N-Methyl-D-Aspartate-Induced Glutathione Efflux in Organotypic Hippocampal Cultures

Journal article
Authors Camilla Wallin
Abdul-Karim Abbas
Mattias Tranberg
Stephen G. Weber
Holger Wigström
Mats Sandberg
Published in Neurochemical Research
Volume 28
Issue 2
Pages 281–291
ISSN 0364-3190
Publication year 2003
Published at Institute of Anatomy and Cell Biology
Institute of Physiology and Pharmacology, Dept of Medical Biophysics
Pages 281–291
Language en
Keywords NMDA; glutathione; phosphoethanolamine; taurine; efflux
Subject categories Neurobiology, Neuroscience, Neurochemistry


N-Methyl-D-aspartate (NMDA)-receptor stimulation evoked a selective and partly delayed elevated efflux of glutathione, phosphoethanolamine, and taurine from organotypic rat hippocampus slice cultures. The protein kinase inhibitors H9 and staurosporine had no effect on the efflux. The phospholipase A2 inhibitors quinacrine and 4-bromophenacyl bromide, as well as arachidonic acid, a product of phospholipase A2 activity, did not affect the stimulated efflux. Polymyxin B, an antimicrobal agent that inhibits protein kinase C, and quinacrine in high concentration (500 microM), blocked efflux completely. The stimulated efflux after but not during NMDA incubation was attenuated by a calmodulin antagonist (W7) and an anion transport inhibitor (DNDS). Omission of calcium increased the spontaneous efflux with no or small additional effects by NMDA. In conclusion, NMDA receptor stimulation cause an increased selective efflux of glutathione, phosphoethanolamine and taurine in organotypic cultures of rat hippocampus. The efflux may partly be regulated by calmodulin and DNDS sensitive channels.

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