Exercise after spinal cord injury as an agent for neuroprotection, regeneration and rehabilitation

Abstract

Spinal cord injury (SCI) is a traumatic event from which there is limited recovery of function, despite the best efforts of many investigators to devise realistic therapeutic treatments. Partly this is due to the multifaceted nature of SCI, where there is considerable disarray and dysfunction secondary to the initial injury. Contributing to this secondary degeneration is neurotoxicity, vascular dysfunction, glial scarring, neuroinflammation, apoptosis and demyelination. It seems logical that addressing the need for neuroprotection, regeneration and rehabilitation will require different treatment strategies that may be applied at varied stages of the post-injury response. Here we focus on a single strategy, exercise/physical training, which appears to have multiple applications and benefits for an acute or chronic SCI. Exercise has been demonstrated to be advantageous at cellular and biochemical levels, as well as being of benefit for the whole animal or human subject. Data from our lab and others will be discussed to further elucidate the many positive aspects of implementing exercise following injury and to suggest that rehabilitation is not the sole target of a training regimen following SCI. This article is part of a Special Issue entitled SI: Spinal cord injury.

Keywords: Exercise; Neurorehabilitation; Neurotrauma; Spinal cord injury.

Figure 1

Passive exercise aids in regulating miRs along with target PTEN expression leading to a decrease in PTEN protein levels (from Liu et al., Exp. Neurol. 233:447–456, 2012).

Figure 2

Passive exercise decreases miR199-3p thereby enabling mTOR mRNA expression and protein levels (from Liu et al., Exp. Neurol. 233:447–456, 2012).

Figure 3

Exercise modulates neurotrophic factor mRNA and neurotrophic factor receptor mRNA expression in motoneurons (from Keeler et al., Brain Research 1438: 8–21, 2012).

Figure 4

Exercise modulates neurotrophic factor mRNA expression but not receptor mRNA in the intermediate grey matter (from Keeler et al., Brain Research 1438: 8–21, 2012).

Figure 5

Bumetanide blocks NKCC1 for H reflex recovery after SCI (from Côté et al., J Neurosci. 34:8976–8987, 2014).

Figure 6

DIOA blocks KCC2, which removes exercise-dependent reflex recovery after injury (from Côté et al., J Neurosci. 34:8976–8987, 2014).

Figure 7

Acute exercise prevents at-level tactile allodynia (from Detloff et al., Exp Neurol. 255:38–48, 2014).

Figure 8

Exercise prevents SCI-induced redistribution of afferents in the ipsilesional dorsal horn responsive to GDNF family of ligands (from Detloff et al., Exp Neurol. 255:38–48, 2014).

Figure 9

Exercise prevents SCI-induced redistribution of afferents in the contralesional dorsal horn responsive to GDNF family of ligands (from Detloff et al., Exp Neurol. 255:38–48, 2014).