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Published on: June 12, 2018
Increased severity of chemically induced seizures in mice with partially deleted Vitamin D receptor gene
Allan V Kalueff1, Anna Minasyan, Tiina Keisala
1Department of Anatomy, Medical School, University of Tampere, Tampere 33014, Finland. avkalueff@inbox.ru
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.
Insights
Vitamin D receptors (VDRs) play a crucial role in modulating seizure susceptibility. VDR knockout mice exhibited increased epilepsy severity, suggesting the Vitamin D/VDR system
Area of Science:
- Neuroendocrinology
- Epilepsy research
- Molecular neuroscience
Background:
- Vitamin D functions as a neuroactive steroid hormone with critical roles in the brain.
- Dysfunctions related to Vitamin D are increasingly linked to epilepsy.
- The specific role of Vitamin D receptors (VDRs) in epilepsy pathogenesis requires further elucidation.
Purpose of the Study:
- To investigate the role of Vitamin D receptors (VDRs) in experimental epilepsy.
- To assess the impact of VDR deficiency on seizure susceptibility and severity in a mouse model.
Main Methods:
- Utilized VDR knockout mice and wild-type littermates for comparison.
- Administered pentylenetetrazole (PTZ) systemically to induce seizures.
- Evaluated seizure profiles, including latency, severity (Racine scores), and mortality rates.
Main Results:
- VDR knockout mice showed significantly shorter latencies to seizure onset compared to wild-type controls.
- VDR knockout mice exhibited higher Racine scores, indicating more severe seizures.
- Mortality rates were increased in the VDR knockout group following PTZ administration.
Conclusions:
- VDRs significantly modulate seizure susceptibility in mice.
- The Vitamin D/VDR endocrine system is implicated in the pathogenesis of epilepsy.
- Targeting the Vitamin D/VDR pathway may offer potential therapeutic strategies for epilepsy.
