Abstracts fromThe 33 ^rd AnnualNational Neurotrauma SymposiumJune 28–July 1, 2015Santa Fe, New Mexico

摘要

Appropriate limb loading is essential for neurorehabilitation after SCI, in part, because it guides spinal cord neuroplasticity. Complete unloading such as prolonged bed rest may interfere with functional recovery, whereas appropriate afferent information through rehabilitation may improve function by modulating spinal plasticity. The impact of limb loading on synaptic plasticity in SCI remains poorly understood. We investigated long-term biological, biomechanical and physiological consequence of hindlimb unloading (HU) in the acute phase of SCI. Adult female SD rats received a mild SCI (T9; 50 kdyn, IH). Three days post-injury, subjects were randomized to two experimental groups: 1) HU by tail suspension, or 2) normal-loading control. After two weeks, the HU group was returned to normal loading condition. Animals were monitored until 8 weeks post-injury. Assessments included: 1) BBB locomotor recovery; 2) kinematic gait analysis; 3) electrophysiological H-reflex testing at 8 weeks-post injury; 4) spinal cord tissue analysis using biomolecular and robotic confocal microscopy assessments of plasticity-related changes in ventral motorneurons. Results indicated that: 1) HU early after SCI impaired recovery of coordinated gait characteristics and produced excessive excitation of spinal reflex circuits; 2) Chronically increased synaptic glutamate AMPA receptors on the plasma membrane of spinal motor neurons providing a cellular mechanism. Our findings suggest that limb unloading early after SCI induces maladaptive spinal cord plasticity that persists to impair functional recovery in chronic phase, providing a novel mechanistic target for early intervention after SCI to enhance the effect of rehabilitation in the chronic phase following injury.