This thesis investigates the postnatal consequences of axon miswiring in the spinal motor system and mechanisms of plasticity that allow for their compensation. I showed that depletion of Npn1 from motor neurons causes severe postnatal defects due to loss of motor axons from the radial nerve. Defective Sema3A-Npn1 binding does not induce the same defects, suggesting that additional binding partners for Npn1 might allow for the compensation of these deficits. Furthermore, I introduced Sema3F mutants as a new, non-injury based model to explore postnatal adaptive plasticity in the motor system. I found evidence for a critical period in which locomotor stimulation can induce neuroanatomical and behavioral adaptations.     «

This thesis investigates the postnatal consequences of axon miswiring in the spinal motor system and mechanisms of plasticity that allow for their compensation. I showed that depletion of Npn1 from motor neurons causes severe postnatal defects due to loss of motor axons from the radial nerve. Defective Sema3A-Npn1 binding does not induce the same defects, suggesting that additional binding partners for Npn1 might allow for the compensation of these deficits. Furthermore, I introduced Sema3F muta...     »