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Elevated Plus Maze for Mice
Published on: December 22, 2008
Slitrk1-deficient mice display elevated anxiety-like behavior and noradrenergic abnormalities.
K Katayama1, K Yamada, V G Ornthanalai
1Laboratory for Behavioral and Developmental Disorders, RIKEN Brain Science Institute, Wako-shi, Saitama, Japan.
Molecular Psychiatry
|September 17, 2008
Summary
Slitrk1 protein deficiency in mice leads to increased anxiety and altered neurochemistry. This suggests noradrenergic mechanisms may underlie Tourette
Area of Science:
- Neuroscience
- Genetics
- Behavioral Science
Background:
- Mutations in SLITRK1 gene are linked to Tourette's syndrome and trichotillomania.
- SLITRK1 encodes a transmembrane protein predominantly expressed in the nervous system.
- The in vivo function of SLITRK1 remains largely uncharacterized.
Purpose of the Study:
- To investigate the in vivo role of Slitrk1.
- To analyze the behavioral and neurochemical phenotypes of Slitrk1-deficient mice.
Main Methods:
- Generation of Slitrk1-knockout mouse model.
- Behavioral testing including elevated plus-maze, forced swimming, and tail suspension tests.
- Neurochemical analysis of neurotransmitter levels.
Main Results:
- Slitrk1-deficient mice displayed heightened anxiety-like behaviors and increased immobility.
- Elevated levels of norepinephrine and its metabolite were observed in knockout mice.
- Clonidine treatment reduced anxiety-like behavior in Slitrk1-deficient mice.
Conclusions:
- Noradrenergic mechanisms are implicated in the behavioral abnormalities associated with Slitrk1 deficiency.
- Slitrk1 dysfunction and resulting anxiety may contribute to the pathogenesis of neuropsychiatric disorders.
- This study provides in vivo evidence for Slitrk1's role in regulating anxiety and neurotransmission.
