Natural Progression of Spinal Cord Transection Injury and Reorganization of Neural Pathways

Abstract

The spinal cord injury (SCI) transection model accurately represents traumatic laceration and has been widely used to study the natural history and reorganization of neuropathways and plasticity in the central nervous system (CNS). This model is highly reproducible, which makes it ideal for studying the progression of injury as well as endogenous recovery and plasticity in the CNS. Five experimental groups of transection injury were designed: left hemitransection; right hemitransection; double hemitransection; complete transection injuries; and laminectomy-only control. We used somatosensory evoked potentials (SSEPs) as an objective electrophysiological assessment tool and motor behavior testing (Basso, Beattie, and Bresnahan [BBB] scoring) to functionally assess the neural pathways post-injury. Histological examinations were carried out to investigate the extent of injury and spinal cord morphological changes. Significant (p < 0.05) electrophysiological changes were observed and were verified by an increase in SSEP amplitude in somatosensory cortices for all four injury groups during days 4 and 7 post-injury. Degree of plasticity among the groups was distinguished by changes in SSEP amplitude and BBB scores. Our results support our previous published findings (using a contusive model of SCI), which shows that the reorganization of neuropathways and plasticity persist in time and are not transient phenomena. SSEPs are a reliable tool to assess the functionality of neural pathways and their projections to higher CNS structures such as the cortices. They enable us to determine residual function and the changes within the CNS post-injury and consistently track these events over time. The results from our study provide supporting evidence for the presence of neuronal network reorganization and plasticity in the CNS after transection SCI.

Characterization of transection spinal cord injuries by monitoring somatosensory evoked potentials and motor behavior

“…Although axons in the adult central nervous system (CNS) lack a noticeable ability to regenerate and repair, some degree of endogenous recovery is possible in both complete and incomplete cases of spinal cord injury (SCI) (Bazley et al, 2011;Vipin et al, 2016;Kirshblum et al, 2011;Bazley et al, 2012). Such functional recovery is generally the result of post-injury adaptive responses in the CNS, namely neural reorganization and plasticity (Bazley et al, 2011;Vipin et al, 2016;Bazley et al, 2014).…”

“…Although axons in the adult central nervous system (CNS) lack a noticeable ability to regenerate and repair, some degree of endogenous recovery is possible in both complete and incomplete cases of spinal cord injury (SCI) (Bazley et al, 2011;Vipin et al, 2016;Kirshblum et al, 2011;Bazley et al, 2012). Such functional recovery is generally the result of post-injury adaptive responses in the CNS, namely neural reorganization and plasticity (Bazley et al, 2011;Vipin et al, 2016;Bazley et al, 2014). Mostly, these reorganizations are associated with the sprouting and rewiring of surviving neurons, as have been observed in several axonal tracts systems, including the corticospinal, reticulospinal and propriospinal tract (Bareyre et al, 2004;Filli and Schwab, 2015;Ballermann and Fouad, 2006).…”

A Time-Course Study of the Expression Level of Synaptic Plasticity-Associated Genes in Un-Lesioned Spinal Cord and Brain Areas in a Rat Model of Spinal Cord Injury: A Bioinformatic Approach

“…These studies have also provided the background and the appropriate endpoint to evaluate efficacy of neuro-rehabilitation and neurostimulation protocols [52], evoking "neuroplasticity" as possible mechanism [7]. The gene expression regulation that we observed in our experiment possibly reflects the deep reorganization of motor pathways that starts immediately after injury [53,54].…”

Unlocking the Recovery Potential: JMJD3 Inhibition-Mediated SAPK/JNK Signaling Inactivation Supports Endogenous Oligodendrocyte-Lineage Commitment Post Mammalian Spinal Cord Injury

“…The mice thoracic hemi-transection SCI model (T9 level, right side) was established according to previous studies [17]. Briefly, the mice were deeply anesthetized with 0.1 ml/10 g of 5% chloral hydrate via intraperitoneal injection.…”