Chronic treatment with glutaric acid induces partial tolerance to excitotoxicity in neuronal cultures from chick embryo telencephalons
Glutaryl-CoA dehydrogenase deficiency (GDD) is characterized biochemically by an accumulation of glutaric (GA) and 3-hydroxyglutaric (3-OH-GA) acids and clinically by the development of acute striatal degeneration. 3-OH-GA was recently shown to induce neuronal damage via N-methyl-D-aspartate (NMDA)...
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| Hauptverfasser: | , , , , , , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
05 April 2002
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| In: |
Journal of neuroscience research
Year: 2002, Jahrgang: 68, Heft: 4, Pages: 424-431 |
| ISSN: | 1097-4547 |
| DOI: | 10.1002/jnr.10189 |
| Online-Zugang: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1002/jnr.10189 Verlag, lizenzpflichtig, Volltext: https://onlinelibrary.wiley.com/doi/abs/10.1002/jnr.10189 
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| Verfasserangaben: | Stefan Kölker, Jürgen G. Okun, Barbara Ahlemeyer, Angela T.S. Wyse, Friederike Hörster, Moacir Wajner, Dirk Kohlmüller, Ertan Mayatepek, Josef Krieglstein, Georg F. Hoffmann |
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| 100 | 1 | |a Kölker, Stefan |e VerfasserIn |0 (DE-588)1022937758 |0 (DE-627)717335771 |0 (DE-576)366197568 |4 aut | |
| 245 | 1 | 0 | |a Chronic treatment with glutaric acid induces partial tolerance to excitotoxicity in neuronal cultures from chick embryo telencephalons |c Stefan Kölker, Jürgen G. Okun, Barbara Ahlemeyer, Angela T.S. Wyse, Friederike Hörster, Moacir Wajner, Dirk Kohlmüller, Ertan Mayatepek, Josef Krieglstein, Georg F. Hoffmann |
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| 520 | |a Glutaryl-CoA dehydrogenase deficiency (GDD) is characterized biochemically by an accumulation of glutaric (GA) and 3-hydroxyglutaric (3-OH-GA) acids and clinically by the development of acute striatal degeneration. 3-OH-GA was recently shown to induce neuronal damage via N-methyl-D-aspartate (NMDA) receptors. The pathogenetic role of GA, however, remains unclear. We demonstrate that GA exerts a dual action in cultured chick embryo neurons. Short-term incubation with millimolar concentrations of GA induces a weak neuronal damage, adding to 3-OH-GA neurotoxicity. In contrast, chronic treatment with subtoxic, micromolar concentrations of GA results in partial tolerance to 3-OH-GA- and NMDA-induced cell damage. A downregulation of NMDA receptors, in particular of the NR2B subunit, is critically involved in this GA-induced effect, resulting in a reduced Ca2+ increase and generation of reactive oxygen species after acute exposure to NMDA or 3-OH-GA. Furthermore, GA decreases Na+/K+-ATPase activity, which is prevented by glutathione, suggesting a modulation of NMDA receptor function via resting membrane potential and Na+-dependent glutamate transport. In contrast, GA does not inhibit mitochondrial respiratory chain and β-oxidation of fatty acids, virtually excluding an activation of NMDA receptors secondary to ATP depletion. These results strongly suggest that GA modulates the NMDA receptor-mediated neurotoxicity of 3-OH-GA, providing an explanatory basis for the non-linear relationship between organic acid concentrations and disease progression in GDD patients. Furthermore, GA-induced downregulation of NMDA receptors might be involved in the delayed cerebral maturation of GDD patients, resulting in frontotemporal atrophy and a reduced opercularization, which are common neuroradiological findings in GDD patients. © 2002 Wiley-Liss, Inc. | ||
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