Research into mechanisms of interaction between growth and inhibitory proteins of the CNS and behavioral expressions of healthy and disordered brain is one of the contemporary topics. A knockdown model with decreased expression of Nogo-A protein in neurons was developed on the genetic background of Sprague-Dawley wildtypes. Disruption of this inhibitory factor was hypothesized to result in behavioral abnormalities, which were studied both in young, middle age (6 months) and aged (12 months) rats.

Animals were tested in a battery of Carousel maze variants with various demands for segregation of spatial information and flexibility; animals avoided an unmarked sector of either stable or rotating arena; moreover the sector could be defined in room- or arena-frame. A shortened Carousel maze battery and Morris water maze (MWM) including one- trial matching-to-place and reversal configurations was used.

Nogo-A-deficient rats were impaired in the final phases of the Carousel maze battery but their spatial working memory tested in the MWM was intact. Middle-aged and aged groups were differently affected in the battery, but deficits in young animals were observed not to be worsened with ageing. Concept of multidirectional age-related alterations in this animal model is further supported by biochemical brain changes.

Nogo-A-deficient rats may serve as an extremely useful model of neurodevelopmental deficit, which may manifest by behavioral changes accessible to phenotyping and in-depth analysis. Relevance of this approach for animal models of neuropsychiatric models will be discussed.