scholarly journals Treadmill exercise facilitates recovery of locomotor function through axonal regeneration following spinal cord injury in rats

2016 ◽  
Vol 12 (4) ◽  
pp. 284-292 ◽  
Author(s):  
Sun-Young Jung ◽  
Tae-Beom Seo ◽  
Dae-Young Kim
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Axonal Regeneration ◽  
Treadmill Exercise ◽  
Locomotor Function ◽  
Cord Injury

Spinal Cord Injury: Lessons from Locomotor Recovery and Axonal Regeneration in Lower Vertebrates

1998 ◽  
Vol 4 (4) ◽  
pp. 250-263 ◽  
Author(s):  
Andrew D. McClellan
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Neural Development ◽  
Axonal Regeneration ◽  
Spinal Cord Injuries ◽  
Axonal Guidance ◽  
Behavioral Recovery ◽  
Locomotor Function ◽  
Cord Injury ◽  
Lower Vertebrates

After severe spinal cord injury in adult higher vertebrates (birds and mammals), there normally is little or no axonal regeneration and virtually no recovery of voluntary locomotor function below the lesion. In contrast, certain lower vertebrates, including lamprey, fish, and some amphibians, exhibit robust axonal regeneration and substantial recovery of locomotor function after spinal cord injury. The remarkable behavioral recovery of lower vertebrates with spinal cord injuries is due to at least three factors: 1) minimal hemorrhagic necrosis at the injury site and the lack of a neurite growth–inhibiting astrocytic scar, 2) an environment in the spinal cord that is permissive for axonal regeneration, and 3) mechanisms for directed axonal elongation and selection of appropriate postsynaptic targets. The latter two features probably represent developmental mechanisms for axonal guidance and synaptogenesis that persist in the nervous systems of these animals well beyond the main phase of neural development. In the injured spinal cords of higher vertebrates, the full complement of manipulations necessary to promote functional regeneration and behavioral recovery is unknown. An understanding of the mechanisms that result in repair of spinal cord injuries in lower vertebrates may provide guidelines for identifying the requirements for functional spinal cord regeneration in higher vertebrates, including humans.

scholarly journals Neuromodulatory effects of repetitive transcranial magnetic stimulation on neural plasticity and motor functions in rats with an incomplete spinal cord injury: A preliminary study

PLoS ONE ◽  
2021 ◽  
Vol 16 (6) ◽  
pp. e0252965
Author(s):  
Siti Ainun Marufa ◽  
Tsung-Hsun Hsieh ◽  
Jian-Chiun Liou ◽  
Hsin-Yung Chen ◽  
Chih-Wei Peng
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Transcranial Magnetic Stimulation ◽  
Axonal Regeneration ◽  
Magnetic Stimulation ◽  
Time Course ◽  
Preclinical Model ◽  
Incomplete Spinal Cord Injury ◽  
Locomotor Function ◽  
Cord Injury

We investigated the effects of intermittent theta-burst stimulation (iTBS) on locomotor function, motor plasticity, and axonal regeneration in an animal model of incomplete spinal cord injury (SCI). Aneurysm clips with different compression forces were applied extradurally around the spinal cord at T10. Motor plasticity was evaluated by examining the motor evoked potentials (MEPs). Long-term iTBS treatment was given at the post-SCI 5th week and continued for 2 weeks (5 consecutive days/week). Time-course changes in locomotor function and the axonal regeneration level were measured by the Basso Beattie Bresnahan (BBB) scale, and growth-associated protein (GAP)-43 expression was detected in brain and spinal cord tissues. iTBS-induced potentiation was reduced at post-1-week SCI lesion and had recovered by 4 weeks post-SCI lesion, except in the severe group. Multiple sessions of iTBS treatment enhanced the motor plasticity in all SCI rats. The locomotor function revealed no significant changes between pre- and post-iTBS treatment in SCI rats. The GAP-43 expression level in the spinal cord increased following 2 weeks of iTBS treatment compared to the sham-treatment group. This preclinical model may provide a translational platform to further investigate therapeutic mechanisms of transcranial magnetic stimulation and enhance the possibility of the potential use of TMS with the iTBS scheme for treating SCIs.

scholarly journals Exercise Ameliorates Spinal Cord Injury by Changing DNA Methylation

Cells ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 143
Author(s):  
Ganchimeg Davaa ◽  
Jin Young Hong ◽  
Tae Uk Kim ◽  
Seong Jae Lee ◽  
Seo Young Kim ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Motor Cortex ◽  
Functional Recovery ◽  
Treadmill Exercise ◽  
Exercise Group ◽  
Control Group ◽  
Epigenetic Changes ◽  
Cord Injury ◽  
The Brain

Exercise training is a traditional method to maximize remaining function in patients with spinal cord injury (SCI), but the exact mechanism by which exercise promotes recovery after SCI has not been identified; whether exercise truly has a beneficial effect on SCI also remains unclear. Previously, we showed that epigenetic changes in the brain motor cortex occur after SCI and that a treatment leading to epigenetic modulation effectively promotes functional recovery after SCI. We aimed to determine how exercise induces functional improvement in rats subjected to SCI and whether epigenetic changes are engaged in the effects of exercise. A spinal cord contusion model was established in rats, which were then subjected to treadmill exercise for 12 weeks. We found that the size of the lesion cavity and the number of macrophages were decreased more in the exercise group than in the control group after 12 weeks of injury. Immunofluorescence and DNA dot blot analysis revealed that levels of 5-methylcytosine (5mC) and 5-hydroxymethylcytosine (5hmC) in the brain motor cortex were increased after exercise. Accordingly, the expression of ten-eleven translocation (Tet) family members (Tet1, Tet2, and Tet3) in the brain motor cortex also elevated. However, no macrophage polarization was induced by exercise. Locomotor function, including Basso, Beattie, and Bresnahan (BBB) and ladder scores, also improved in the exercise group compared to the control group. We concluded that treadmill exercise facilitates functional recovery in rats with SCI, and mechanistically epigenetic changes in the brain motor cortex may contribute to exercise-induced improvements.

scholarly journals Chemotropic guidance facilitates axonal regeneration and synapse formation after spinal cord injury

2009 ◽  
Vol 12 (9) ◽  
pp. 1106-1113 ◽  
Author(s):  
Laura Taylor Alto ◽  
Leif A Havton ◽  
James M Conner ◽  
Edmund R Hollis II ◽  
Armin Blesch ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Axonal Regeneration ◽  
Synapse Formation ◽  
Cord Injury

scholarly journals Descending propriospinal neurons mediate restoration of locomotor function following spinal cord injury

2017 ◽  
Vol 117 (1) ◽  
pp. 215-229 ◽  
Author(s):  
Katelyn N. Benthall ◽  
Ryan A. Hough ◽  
Andrew D. McClellan
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Axonal Regeneration ◽  
Central Pattern Generators ◽  
Burst Activity ◽  
Compensatory Mechanism ◽  
Spinal Lesions ◽  
Cord Injury ◽  
Recovery Times ◽  
Indirect Activation

Following spinal cord injury (SCI) in the lamprey, there is virtually complete recovery of locomotion within a few weeks, but interestingly, axonal regeneration of reticulospinal (RS) neurons is mostly limited to short distances caudal to the injury site. To explain this situation, we hypothesize that descending propriospinal (PS) neurons relay descending drive from RS neurons to indirectly activate spinal central pattern generators (CPGs). In the present study, the contributions of PS neurons to locomotor recovery were tested in the lamprey following SCI. First, long RS neuron projections were interrupted by staggered spinal hemitransections on the right side at 10% body length (BL; normalized from the tip of the oral hood) and on the left side at 30% BL. For acute recovery conditions (≤1 wk) and before axonal regeneration, swimming muscle burst activity was relatively normal, but with some deficits in coordination. Second, lampreys received two spaced complete spinal transections, one at 10% BL and one at 30% BL, to interrupt long-axon RS neuron projections. At short recovery times (3–5 wk), RS and PS neurons will have regenerated their axons for short distances and potentially established a polysynaptic descending command pathway. At these short recovery times, swimming muscle burst activity had only minor coordination deficits. A computer model that incorporated either of the two spinal lesions could mimic many aspects of the experimental data. In conclusion, descending PS neurons are a viable mechanism for indirect activation of spinal locomotor CPGs, although there can be coordination deficits of locomotor activity. NEW & NOTEWORTHY In the lamprey following spinal lesion-mediated interruption of long axonal projections of reticulospinal (RS) neurons, sensory stimulation still elicited relatively normal locomotor muscle burst activity, but with some coordination deficits. Computer models incorporating the spinal lesions could mimic many aspects of the experimental results. Thus, after disruption of long-axon projections from RS neurons in the lamprey, descending propriospinal (PS) neurons appear to be a viable compensatory mechanism for indirect activation of spinal locomotor networks.

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