Treadmill training promotes spinal changes leading to locomotor recovery after partial spinal cord injury in cats

Abstract

After a spinal hemisection at thoracic level in cats, the paretic hindlimb progressively recovers locomotion without treadmill training but asymmetries between hindlimbs persist for several weeks and can be seen even after a further complete spinal transection at T13. To promote optimal locomotor recovery after hemisection, such asymmetrical changes need to be corrected. In the present study we determined if the locomotor deficits induced by a spinal hemisection can be corrected by locomotor training and, if so, whether the spinal stepping after the complete spinal cord transection is also more symmetrical. This would indicate that locomotor training in the hemisected period induces efficient changes in the spinal cord itself. Sixteen adult cats were first submitted to a spinal hemisection at T10. One group received 3 wk of treadmill training, whereas the second group did not. Detailed kinematic and electromyographic analyses showed that a 3-wk period of locomotor training was sufficient to improve the quality and symmetry of walking of the hindlimbs. Moreover, after the complete spinal lesion was performed, all the trained cats reexpressed bilateral and symmetrical hindlimb locomotion within 24 h. By contrast, the locomotor pattern of the untrained cats remained asymmetrical, and the hindlimb on the side of the hemisection was still deficient. This study highlights the beneficial role of locomotor training in facilitating bilateral and symmetrical functional plastic changes within the spinal circuitry and in promoting locomotor recovery after an incomplete spinal cord injury.

Treadmill training induced lumbar motoneuron dendritic plasticity and behavior recovery in adult rats after a thoracic contusive spinal cord injury

“…Given that BDNF can act locally on the motoneuron soma as well as through dendritic transport (Rind et al, 2005), such upregulation could potentiate both protective and dendritic growth effects in the motoneuron pools of these hindlimb muscles. Also, BDNF can be produced within the musculature itself and retrogradely transported to exert effects on the innervating motoneuron (Martinez et al, 2013;West et al, 2014). BDNF has been shown to enhance dendritic complexity and synapse formation in vitro and in vivo.…”

“…In reality, individuals with complete motor SCI with an American Spinal Injury Association Level A (ASIA-A) are not likely to recover locomotor function post-injury (Lunenburger et al, 2006). However, active exercise and rehabilitation regimens have demonstrated some success at restoring locomotor ability in incomplete SCI, and that altered neural plasticity may contribute to recovery (Jung et al, 2014;Martinez et al, 2013;Shin et al, 2014;Yang et al, 2014). Previous studies have applied targeted exercise or rehabilitation regimens spanning 5-6 weeks upon initiation of SCI (Shah et al, 2012(Shah et al, , 2013Weishaupt et al, 2013) though some locomotorbased training models have extended to 12 weeks in length (Multon et al, 2003).…”

Functional recovery in spinal cord injured rats using polypyrrole/iodine implants and treadmill training

“…Moreover, active exercise performed mainly by locomotor training treadmill (TT) with or without partial body-weight support or robotic or manual assistance, has been shown to not only enhance locomotor function in both experimental and clinical studies but to also induce plasticity [27][28][29]. Therefore, to preserve the greatest amount of spinal cord tissue and to induce the neuroregenerative processes with the aim to obtain a higher functional recovery rate, the present study proposes the use of implants of PPy/I synthesized by plasma in therapeutic combination with TT for the treatment of a TSCI produced by contusion in rats.…”

Desenvolvimento de caminhar espinal em cães paraplégicos com fraturas e luxações vertebrais toracolombares

“…O surgimento de atividade motora nesses cães pode ser indicativo do desenvolvimento de caminhar espinal reflexo, originado do mecanismo de plasticidade neuronal, da formação de circuitos de regulação central medular induzidos por movimentos repetitivos, do desenvolvimento de espasticidade muscular ou da ação de axônios sobreviventes que atravessam o sítio da lesão e permitem que o animal execute movimentos deambulatórios de forma involuntá-ria (Freeman 1952, Dietz 2001, Pearson 2001, Olby et al 2003, Araújo et al 2009, Rossignol et al 2009& Martinez et al 2013, Wittler 2014, Dewey 2016.…”

“…Estudos eletrofisiológicos e histológicos têm demonstrado a criação de circuitos de regulação central medular, que podem ser condicionados por estímulos repetitivos para regular o caminhar espinal (Dietz 2001, Behrman et al 2006, Barrière et al 2008, Rossignol et al 2009, Frigon 2012, Martinez et al 2013.…”