Exoskeleton training was generally safe and feasible in a heterogeneous sample of persons with SCI. Results indicate potential benefits on gait function and balance.

We have studied the axonal projection patterns of commissural interneurons (CINs) in the neonatal rat spinal cord. Some CINs are integral components of the neuronal networks in the vertebrate spinal cord that generate locomotor activity. By using differential retrograde labeling protocols with fluorescent dextran amines, we show that CINs with ascending axons (ascending CINs, or aCINs) and CINs with descending axons (descending CINs, or dCINs) constitute largely different populations. We show that aCINs and dCINs occupy partially overlapping domains in the transverse plane. The aCINs are located at the dorsal margin, within the dorsal horn, centrally within the intermediate zone, and in the medial region of the ventral horn, whereas the dCINs are located predominantly among the ventral and central aCINs and in smaller numbers within the dorsal horn. The labeled aCINs and dCINs project for at least one and a half segment rostrally or caudally and are present in roughly equal numbers. We also demonstrate the presence of a third, smaller population of CINs whose axons bifurcate to project for at least one and a half segment both rostrally and caudally (adCINs). The adCINs are located predominantly among the central and ventral groups of aCINs and dCINs. Finally, we demonstrate the presence of CINs with axons projecting for fewer than one and a half segment in either direction. These "short-range CINs" are intermingled with the aCINs, dCINs, and adCINs. Our results provide an anatomical framework for further electrophysiological studies aimed at identifying the CINs that participate in the mammalian locomotor central pattern generator.

Training seemed not to provoke new pain. Spasticity decreased after a single training session. SCIM III and quality of life increased longitudinally for subsets of participants.

Signaling by receptor tyrosine kinases (RTKs) is mediated by their intrinsic kinase activity. Typically, kinase-activating mutations result in ligand-independent signaling and gain-of-function phenotypes. Like other RTKs, Ephs require kinase activity to signal, but signaling by Ephs in vitro also requires clustering by their membrane bound ephrin ligands. The relative importance of Eph kinase activity and clustering for in vivo functions is unknown. We find that knockin mice expressing a mutant form of EphA4 (EphA4(EE)), whose kinase is constitutively activated in the absence of ephrinB ligands, are deficient in the development of thalamocortical projections and some aspects of central pattern generator rhythmicity. Surprisingly, other functions of EphA4 were regulated normally by EphA4(EE), including midline axon guidance, hindlimb locomotion, in vitro growth cone collapse, and phosphorylation of ephexin1. These results suggest that signaling of Eph RTKs follows a multistep process of induced kinase activity and higher-order clustering different from RTKs responding to soluble ligands.