RESUMEN
Spinal cord injury (SCI) disrupts communication between the brain-derived descending commands and the intraspinal circuits, the central pattern generator (CPG), that execute movements. Dynamic changes in the interaction of the brain-spinal cord as well as in structure-function relationships play a vital role in the determination of neurological function restoration. These changes also have important clinical implications for the treatment of patients with SCI. After SCI, at both brain and spinal cord levels, detour circuits formation and neuronal plasticity have been linked to functional improvement under the condition of spontaneous recovery as well as electrical stimulation- and rehabilitative training-assisted recovery. The principles governing neural circuit remodeling and the neuronal subtypes specifically involved during the recovery from SCI are largely unknown. In the present review, we focus on how multi-level neural circuits are reconstructed after SCI. We highlight some new studies using rodent and zebrafish SCI models that describe how the intraspinal detour circuits are reconstructed and the important roles of spinal excitatory interneurons.
RESUMEN
Studies conducted since the second half of the 19th century have revealed spontaneous as well as pharmacologically induced phasic/rhythmic discharge in spinal respiratory motor outputs of cats, dogs, rabbits, and neonatal rats following high cervical transection (Tx). The extent to which these various studies validate the existence of a true spinal respiratory rhythm generator remains debated. In this set of studies, we seek to characterize patterns of spontaneous phasic/rhythmic, asphyxia-induced, and pharmacologically induced activity occurring in phrenic nerve (PhN) discharge after complete high cervical (C1-C2) spinal cord transection. Experiments were performed on 20 unanesthetized decerebrate Sprague-Dawley adult male rats. Patterns of spontaneous activity after spinalization included tonic, phasic, slow oscillatory, and long-lasting tonic discharges. Topical application of antagonists of GABAA and glycine receptors to C1- and C2- spinal segments induced left-right synchronized phasic decrementing activity in PhN discharge that was abolished by an additional C2Tx. Asphyxia elicited increases in tonic activity and left-right synchronized gasp-like bursts in PhN discharge, demonstrating the presence of spinal circuits that may underlie a spinal gasping-like mechanism. We conclude that intrinsic slow oscillators and a phasic burst/rhythm generator exist in the spinal cord of the adult rat. If present in humans, this mechanism may be exploited to recover respiratory function in patients sustaining severe spinal cord injury.