Transient protective effect of B-vitamins in experimental epilepsy in the mouse brain
The regulation of programmed cell death in the nervous system of vertebrates is a complex mechanism aimed to remove superfluous or damaged cells. Epileptic seizures can lead to an activation of pathways resulting in neuronal cell death. B-vitamins might have a neuroprotective potential reducing cell...
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| Main Authors: | , , , , , , , , |
|---|---|
| Format: | Article (Journal) |
| Language: | English |
| Published: |
May 2010
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| In: |
Journal of molecular neuroscience
Year: 2009, Volume: 41, Issue: 1, Pages: 74-79 |
| ISSN: | 1559-1166 |
| DOI: | 10.1007/s12031-009-9286-4 |
| Online Access: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1007/s12031-009-9286-4 |
| Author Notes: | Tamer Rabie, Wolfgang Mühlhofer, Thomas Bruckner, Anna Schwab, Alexander T. Bauer, Manfred Zimmermann, Dieter Bonke, Hugo H. Marti, Johannes Schenkel |
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| 245 | 1 | 0 | |a Transient protective effect of B-vitamins in experimental epilepsy in the mouse brain |c Tamer Rabie, Wolfgang Mühlhofer, Thomas Bruckner, Anna Schwab, Alexander T. Bauer, Manfred Zimmermann, Dieter Bonke, Hugo H. Marti, Johannes Schenkel |
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| 520 | |a The regulation of programmed cell death in the nervous system of vertebrates is a complex mechanism aimed to remove superfluous or damaged cells. Epileptic seizures can lead to an activation of pathways resulting in neuronal cell death. B-vitamins might have a neuroprotective potential reducing cell death following appropriate stimulation. Here, the role of the B-vitamins B1 (thiamine), B6 (pyridoxine), and B12 (cobalamine) was investigated in a mouse model of experimental epilepsy induced by kainate. B-vitamin pre-treated animals showed a significantly reduced epileptic score during the first 15 min after kainate injection. The molecular response to kainate showed a bi-phased time course with early induction of Bcl-2 expression within 12 h and a second induction after 7 days of kainate exposure. B-vitamin pre-treatment resulted in significant higher Bcl-2 expression in control animals (no kainate) and at 12 h within the early phase. Bcl-2 expression was not affected by B-vitamins within the second phase. BAX expression was not significantly influenced during the whole experiment. Three days after kainate stimulation, the number of TdT-mediated dUTP-biotin nick end labeling-positive cells in the hippocampal region was lower in B-vitamin-treated animals. Therefore, B-vitamin pre-treatment may attenuate the response to epileptic stimulation. | ||
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