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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: Rabie, Tamer (Author) , Mühlhofer, Wolfgang Gerhard (Author) , Bruckner, Thomas (Author) , Schwab, Anna (Author) , Bauer, Alexander (Author) , Zimmermann, Manfred (Author) , Bonke, Dieter (Author) , Marti, Hugo (Author) , Schenkel, Johannes (Author)
Format: Article (Journal)
Language:English
Published: May 2010
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
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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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Summary: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.
Item Description:Published online: 24 September 2009
Gesehen am 04.05.2021
Physical Description:Online Resource
ISSN:1559-1166
DOI:10.1007/s12031-009-9286-4

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