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Comprehensive behavioral study of mGluR3 knockout mice: implication in schizophrenia related endophenotypes
Ryuta Fujioka, Takenobu Nii, Akiko Iwaki
1Division of Human Molecular Genetics, Research Center for Genetic Information, Medical Institute of Bioregulation, Fukuoka 812-8582, Japan. yfukumak@gen.kyushu-u.ac.jp.
Molecular Brain
|April 25, 2014
Summary
Mice lacking the GRM3 gene (metabotropic glutamate receptor 3) exhibited schizophrenia-like behaviors, including hyperactivity and memory deficits. This suggests a link between glutamate signaling and schizophrenia pathophysiology.
Area of Science:
- Neuroscience
- Genetics
- Psychiatry
Background:
- Previous studies linked GRM3 gene polymorphisms to schizophrenia.
- The precise function of GRM3 in brain and schizophrenia pathogenesis is unclear.
Purpose of the Study:
- To investigate the role of GRM3 in brain function and schizophrenia-like behaviors.
- To explore the impact of GRM3 deficiency on behavior and synaptic plasticity.
Main Methods:
- Generated GRM3 knockout (KO) mice for behavioral analysis.
- Assessed memory, hyperactivity, and long-term potentiation (LTP).
- Measured dopamine release in the nucleus accumbens using in vivo microdialysis.
Main Results:
- GRM3 KO mice displayed hyperactivity and impaired working, contextual, and reference memory.
- No significant difference in hippocampal LTP was observed between KO and wild-type mice.
- KO mice showed enhanced dopamine release in response to methamphetamine.
Conclusions:
- GRM3 deficiency leads to schizophrenia-like behaviors in mice.
- Disrupted glutamate-dopamine interactions may contribute to schizophrenia pathophysiology.
