NOGO-66 receptor deficient mice show slow acquisition of spatial memory task performance

• Published in: Neuroscience letters 2012-02, Vol.510 (1), p.58-61
• Main Authors: van Gaalen, Marcel M., Relo, Ana L., Mueller, Bernhard K., Gross, Gerhard, Mezler, Mario
• Format: Article
• Language: English
• Subjects: Alzheimer Disease - drug therapy; Amphetamine - pharmacology; Animals; Cognition; Eating; Female; Fever - etiology; Hyperkinesis - chemically induced; Knock-out; Learning; Male; Maze Learning - drug effects; Memory; Memory - drug effects; Mice; Mice, Inbred C57BL; Myelin Proteins - deficiency; Myelin Proteins - genetics; Neuronal Plasticity; NgR1; Nogo Proteins; Phencyclidine - pharmacology; Restraint, Physical; Schizophrenia; Schizophrenia - chemically induced; Schizophrenia - physiopathology; Time Factors
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/j.neulet.2012.01.004

► ngr−/− mice does not affect response to amphetamine or PCP. ► ngr−/− animals show slower acquisition of water maze performance. ► Indicating a role in spatial learning and memory. ► Line with the suggested role of NgR1 n plasticity may indicate NgR1 as an interesting drug target for AD. The Nogo-66 receptor (NgR1) is part of a co-receptor complex on neurons that transmits a signal for inhibition of neurite outgrowth. In addition, NgR1 function has also been related to other disorders such as schizophrenia and Alzheimer's disease. Here, we studied the effect of life-long deletion of NgR1 (ngr−/−) in tests for cognition and positive symptoms of schizophrenia. In the water maze, ngr−/− mice learned to locate the hidden platform as well as wild type mice, although with slower acquisition. Deletion of NgR1 did not affect amphetamine- or phencyclidine (PCP)-induced hyperactivity, two models of positive symptoms of schizophrenia. Taken together, ngr−/− animals show slower acquisition of a spatial learning and memory task.