Nogo is a neuronal and myelin membrane protein that inhibits neurite outgrowth and impedes functional recovery after spinal cord injury. Examining the trafficking of nogo and the nogo-66 receptor (NgR) in neuronal cultures will address functions of nogo in regulating axon and dendritic spine formation. Mice lacking a functional gene for nogo display elongation and collateral sprouting of damaged axons, and improved locomotor activity following spinal cord injury (SCI). Understanding the physiological function(s) of nogo in contexts other than SCI may provide opportunities to develop rational interventions for promoting functional recovery from CNS injury. In mice lacking nogo, or NgR, analysis of afferent terminations from dorsal roots adjacent regions of the spinal cord denervated by rhizotomy will determine if nogo or NgR can increase the sprouting of uninjured neurons. The plasticity of the vibrissae (whisker) representations (barrels) in somatosensory cortex may be aberrant these mice. Comparing the pattern of barrels by staining, and neuronal structural plasticity with chronic imaging of cortical pyramidal neurons in these mutant mice may elucidate role of nogo and signaling through the NgR in regulating cortical plasticity.
