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.

Brain Research Institute University of Zürich and Department of Biology ETH Zürich Winterthurerstr 190 8057 Zürich Switzerland

Brain Research Institute University of Zürich and Department of Biology ETH Zürich Winterthurerstr 190 8057 Zürich Switzerland; Division of Molecular Mechanisms of Tumor Invasion German Cancer Research Center Im Neuenheimer Feld 581 69120 Heidelberg Germany

Department of Molecular Biology Central Institute of Mental Health J5 68159 Mannheim Germany

Institute of Physiology Academy of Sciences of the Czech Republic Videnska 1083 14220 Prague 4 Czech Republic

Institute of Physiology Academy of Sciences of the Czech Republic Videnska 1083 14220 Prague 4 Czech Republic; Charles University In Prague 1 Faculty Of Medicine Prague Czech Republic

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