Unlike adult spinalized rats, ~20% of rats spinalized as P1/P2 neonates achieve autonomous hindlimb weight support. Cortical representations of mid/low trunk only occur in such rats with high weight support. However, the importance of hindlimb/trunk motor cortex in function of spinalized rats remains unclear. We tested the importance of trunk sensorimotor cortex in their locomotion using lesions guided by cortical microstimulation in P1/2 weight-supporting neonatal spinalized rats and controls. In 4 intact control rats, lesions of hindlimb/trunk cortex caused no treadmill deficits. All spinalized rats lesioned in trunk cortex (n=16, 4 transplant, 6 transect, 6 transect + fibrin glue,) lost an average of ~40% of their weight support. Intact trunk cortex was essential to their level of function. Lesion of trunk cortex substantially increased roll of the hindquarters, which correlated to diminished weight support, but other kinematic stepping parameters showed little change. E14 transplants support development of the trunk motor representations in their normal location (Giszter et al. 1998). We tested the role of novel relay circuits arising from the grafts in such cortical representations in E14 transplants using the rats that received (non-cellular) fibrin glue grafting at P1/2, (8 allografts, and 32 xenografts). Fibrin repaired rats with autonomous weight-support also had trunk cortical representations similar to E14 transplant rats. Thus, acellular repair and intrinsic plasticity were sufficient to support the observed features. Our data show that effective cortical mechanisms for trunk control are essential for autonomous weight-support in P1/P2 spinalized rats and these can be achieved by intrinsic plasticity.