Journal
BEHAVIOURAL BRAIN RESEARCH
Volume 224, Issue 1, Pages 73-79Publisher
ELSEVIER
DOI: 10.1016/j.bbr.2011.05.020
Keywords
Reticulon-4 receptor; Mouse model; Schizophrenia; PPI; Spatial cognition; Social interaction
Categories
Funding
- National Sciences and Engineering Research Council of Canada [A0669]
- Japan Ministry of Education, Science, Sports and Culture [KAKENHI 15200032, KAKENHI 21240043, KAKENHI20790196]
- Japan Society for the Promotion of Science (JSPS)
- Grants-in-Aid for Scientific Research [21240043] Funding Source: KAKEN
Ask authors/readers for more resources
The reticulon-4 receptor, encoded by RTN4R, limits axonal sprouting and neural plasticity by inhibiting the outgrowth of neurites. Human association studies have implicated mutations in RTN4R in the development of schizophrenia, including the identification of several rare nonconservative missense mutations of RTN4R in schizophrenia patients. To investigate the effects of missense mutation of the reticulon-4 receptor on phenotypes relevant to schizophrenia, we behaviourally characterized a novel Rtn4r mutant mouse line with an amino acid substitution (R189H) in the Nogo-66 binding site. Behavioural assays included prepulse inhibition of acoustic startle, locomotor activity, social interaction and spatial cognition. When compared with wildtype littermates, Rtn4r mutant mice exhibited greater social preference, which may reflect a social-anxyolitic effect, and a mild impairment in spatial cognition. Given the mild effect of the R189H mutation of Rtn4r on behavioural phenotypes relevant to schizophrenia, our results do not support missense mutation of RTN4R as a strong risk factor in the pathogenesis of schizophrenia. (C) 2011 Elsevier B.V. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available