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

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

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

62 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)69-73
Number of pages5
JournalNeuroscience Letters
Volume394
Issue number1
DOIs
Publication statusPublished - 6 Feb 2006
Externally publishedYes

Keywords

  • Chemically induced seizures
  • Epilepsy
  • Knockout mice
  • Vitamin D
  • Vitamin D receptors

Fingerprint

Dive into the research topics of 'Increased severity of chemically induced seizures in mice with partially deleted Vitamin D receptor gene'. Together they form a unique fingerprint.

Cite this