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Nogo-A downregulation impairs place avoidance in the Carousel maze but not spatial memory in the Morris water maze
T. Petrasek, I. Prokopova, S. Bahnik, K. Schonig, S. Berger, K. Vales, B. Tews, ME. Schwab, D. Bartsch, A. Stuchlik,
Language English Country United States
Document type Journal Article, Research Support, Non-U.S. Gov't
Grant support
NT13386
MZ0
CEP Register
- MeSH
- Maze Learning physiology MeSH
- Down-Regulation * MeSH
- Gene Knockdown Techniques MeSH
- Rats MeSH
- Myelin Proteins genetics metabolism MeSH
- Rats, Sprague-Dawley MeSH
- Rats, Transgenic MeSH
- Spatial Behavior physiology MeSH
- Avoidance Learning physiology MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
Nogo-A protein is an important inhibitor of axonal growth, which also regulates neuronal plasticity in the CNS. Mutations in the gene encoding Nogo-A or abnormalities in Nogo-A expression are linked to neuropsychiatric disorders such as schizophrenia. The present study assesses the impact of constitutively reduced expression of Nogo-A on place navigation in a novel transgenic rat model. Two spatial paradigms were used: (1) A battery of tests in the Carousel maze requiring continuous processing of spatial information with increasing demands for the segregation of reference frames and behavioral flexibility and (2) a delayed-matching-to-place version of the Morris water maze (MWM), which requires place navigation and is sensitive to deficits in one-trial-encoded place representation. The Carousel maze testing revealed a subtle but significant impairment in management of reference frames. Matching-to-place learning in the Morris water maze was unaffected, suggesting an intact representation of an unmarked goal. Our results show that Nogo-A deficiency leads to cognitive deficit in processing of the reference frames. Such a deficit may be the result of neuro-developmental alterations resulting from Nogo-A deficiency.
Charles University In Prague 1 Faculty Of Medicine Prague Czech Republic
Department of Molecular Biology Central Institute of Mental Health J5 68159 Mannheim Germany
References provided by Crossref.org
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- $a Nogo-A protein is an important inhibitor of axonal growth, which also regulates neuronal plasticity in the CNS. Mutations in the gene encoding Nogo-A or abnormalities in Nogo-A expression are linked to neuropsychiatric disorders such as schizophrenia. The present study assesses the impact of constitutively reduced expression of Nogo-A on place navigation in a novel transgenic rat model. Two spatial paradigms were used: (1) A battery of tests in the Carousel maze requiring continuous processing of spatial information with increasing demands for the segregation of reference frames and behavioral flexibility and (2) a delayed-matching-to-place version of the Morris water maze (MWM), which requires place navigation and is sensitive to deficits in one-trial-encoded place representation. The Carousel maze testing revealed a subtle but significant impairment in management of reference frames. Matching-to-place learning in the Morris water maze was unaffected, suggesting an intact representation of an unmarked goal. Our results show that Nogo-A deficiency leads to cognitive deficit in processing of the reference frames. Such a deficit may be the result of neuro-developmental alterations resulting from Nogo-A deficiency.
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