Transient protective effect of B-vitamins in experimental epilepsy in the mouse brain

• Verfasst von: Rabie, Tamer [VerfasserIn]
• Verfasst von: Mühlhofer, Wolfgang Gerhard [VerfasserIn]
• Verfasst von: Bruckner, Thomas [VerfasserIn]
• Verfasst von: Schwab, Anna [VerfasserIn]
• Verfasst von: Bauer, Alexander [VerfasserIn]
• Verfasst von: Zimmermann, Manfred [VerfasserIn]
• Verfasst von: Bonke, Dieter [VerfasserIn]
• Verfasst von: Marti, Hugo [VerfasserIn]
• Verfasst von: Schenkel, Johannes [VerfasserIn]
• Titel: Transient protective effect of B-vitamins in experimental epilepsy in the mouse brain
• Verf.angabe: Tamer Rabie, Wolfgang Mühlhofer, Thomas Bruckner, Anna Schwab, Alexander T. Bauer, Manfred Zimmermann, Dieter Bonke, Hugo H. Marti, Johannes Schenkel
• E-Jahr: 2010
• Jahr: May 2010
• Jahr des Originals: 2009
• Umfang: 6 S.
• Fussnoten: Published online: 24 September 2009 ; Gesehen am 04.05.2021
• Titel Quelle: Enthalten in: Journal of molecular neuroscience
• Ort Quelle: New York, NY : Springer, 1998
• Jahr Quelle: 2010
• Band/Heft Quelle: 41(2010), 1, Seite 74-79
• ISSN Quelle: 1559-1166
• DOI: doi:10.1007/s12031-009-9286-4
• Datenträger: Online-Ressource
• Sprache: eng
• K10plus-PPN: 1757062165

Abstract

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.