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Increased severity of chemically induced seizures in mice with partially deleted Vitamin D receptor gene.

作者信息

Kalueff Allan V, Minasyan Anna, Keisala Tiina, Kuuslahti Marianne, Miettinen Susanna, Tuohimaa Pentti

机构信息

Department of Anatomy, Medical School, University of Tampere, Tampere 33014, Finland.

出版信息

Neurosci Lett. 2006 Feb 6;394(1):69-73. doi: 10.1016/j.neulet.2005.10.007. Epub 2005 Oct 25.

DOI:10.1016/j.neulet.2005.10.007
PMID:16256271
Abstract

Vitamin D is a neuroactive steroid hormone with multiple functions in the brain. Numerous clinical and experimental data link various Vitamin D-related dysfunctions to epilepsy. Here, we study the role of Vitamin D receptors (VDRs) in experimental epilepsy in mice. To examine this problem, we assessed the seizure profiles in VDR knockout mice following a systemic injection of pentylenetetrazole (70 mg/kg). Overall, compared to the wild-type (WT) 129S1 mice (n=10 in each group), the VDR knockout group significantly demonstrated shorter latencies to the onset, higher Racine scores and increased mortality rates. Our findings suggest that VDRs modulate seizure susceptibility in mice, and that the Vitamin D/VDR endocrine system may be involved in the pathogenesis of epilepsy.

摘要

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