The Beneficial Effects of Treadmill Step Training on Activity-Dependent Synaptic and Cellular Plasticity Markers After Complete Spinal Cord Injury

Abstract

Several studies have shown that treadmill training improves neurological outcomes and promotes plasticity in lumbar spinal cord of spinal animals. The morphological and biochemical mechanisms underlying these phenomena remain unclear. The purpose of this study was to provide evidence of activity-dependent plasticity in spinal cord segment (L5) below a complete spinal cord transection (SCT) at T8-9 in rats in which the lower spinal cord segments have been fully separated from supraspinal control and that subsequently underwent treadmill step training. Five days after SCT, spinal animals started a step-training program on a treadmill with partial body weight support and manual step help. Hindlimb movements were evaluated over time and scored on the basis of the open-field BBB scale and were significantly improved at post-injury weeks 8 and 10 in trained spinal animals. Treadmill training also showed normalization of withdrawal reflex in trained spinal animals, which was significantly different from the untrained animals at post-injury weeks 8 and 10. Additionally, compared to controls, spinal rats had alpha motoneuronal soma size atrophy and reduced synaptophysin protein expression and Na(+), K(+)-ATPase activity in lumbar spinal cord. Step-trained rats had motoneuronal soma size, synaptophysin expression and Na(+), K(+)-ATPase activity similar to control animals. These findings suggest that treadmill step training can promote activity-dependent neural plasticity in lumbar spinal cord, which may lead to neurological improvements without supraspinal descending control after complete spinal cord injury.

Locomotor training modifies soleus monosynaptic motoneuron responses in human spinal cord injury

“…Animal studies have demonstrated that locomotor training changes the cellular and electrical properties of spinal motoneurons, synaptic inputs, activity of synaptic proteins, ion conductances, and the motoneuronal soma size in the absence of supraspinal descending control (Beaumont et al 2004; Petruska et al 2007; Dunlop 2008; Ilha et al 2011). Further, in people with SCI, motor cortex activation and corticospinal excitability are increased (Dobkin 2000; Winchester et al 2005; Thomas and Gorassini 2005), and cortical facilitation of late flexor reflexes reverses to cortical inhibition (Hajela et al 2013) after locomotor training.…”

Expression of Glutamate and GABA during the Process of Rat Retinal Synaptic Plasticity Induced by Acute High Intraocular Pressure

“…SYN is often considered a marker of presynaptic terminals [13, 18]. SYN is a marker of synapse formation during neural tissue development and is also widely used in the study of synaptic plasticity in nervous system development [20, 34], injury [7, 16] and diseases [5, 29]. Our results were in accordance with a previous study [3, 15] in which SYN expression exhibited a spatiotemporal pattern that was initially successively increased from the IPL to the OPL and then returned to normal.…”

Locomotor training improves reciprocal and nonreciprocal inhibitory control of soleus motoneurons in human spinal cord injury

“…This is supported by the ability of the spinal cord after complete spinalization to undergo functional reorganization with locomotor training (Rossignol 2006) and that the plasticity of the glycinergic system, which mediates inhibitory neurotransmission, can occur independent of supraspinal influences (Sadlaoud et al 2010). Locomotor training normalizes the proportion of inhibitory and excitatory synaptic inputs to spinal motoneurons (Ichiyama et al 2011), improves synaptic inputs from Ia afferents (Petruska et al 2007), alters the concentration levels of Na ϩ -K ϩ -ATPase (Ilha et al 2011), and reverses disynaptic inhibition to polysynaptic excitation (Côté et al 2003) in animals. We have recently shown that locomotor training changes the behavior of short-and long-latency flexion reflexes, reestablishes a physiologic soleus H-reflex phasedependent modulation, increases presynaptic inhibitory control of soleus motoneurons, modifies excitability properties of so- percentage of change of the conditioned H reflex during seated from all subjects after training, reflecting the magnitude of reciprocal and nonreciprocal inhibition, is plotted against the years postinjury.…”