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

Neurosci Lett. 2012 Feb 21;510(1):58-61. doi: 10.1016/j.neulet.2012.01.004. Epub 2012 Jan 11.

Abstract

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.

MeSH terms

  • Alzheimer Disease / drug therapy
  • Amphetamine / pharmacology
  • Animals
  • Eating
  • Female
  • Fever / etiology
  • Hyperkinesis / chemically induced
  • Male
  • Maze Learning* / drug effects
  • Memory* / drug effects
  • Mice
  • Mice, Inbred C57BL
  • Myelin Proteins / deficiency*
  • Myelin Proteins / genetics
  • Neuronal Plasticity
  • Nogo Proteins
  • Phencyclidine / pharmacology
  • Restraint, Physical
  • Schizophrenia / chemically induced
  • Schizophrenia / physiopathology
  • Time Factors

Substances

  • Myelin Proteins
  • Nogo Proteins
  • Rtn4 protein, mouse
  • Amphetamine
  • Phencyclidine