Plasticity of functional connectivity in the adult spinal cord

Cai, L.L.; Courtine, Grégoire; Fong, Andy J.; Burdick, Joel W.; Roy, Roland R.; Edgerton, V. Reggie

doi:10.1098/rstb.2006.1884

Cited by 69 publications

(51 citation statements)

References 72 publications

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“…These data imply that the most effective learning paradigm for spinal cord injured subjects would allow some critical level of variation in stepping kinematics and kinetics (Cai et al, 2006a). We propose that this could be an important feature of the software control that is applied to robotics designed to retrain spinal cord injured subjects to step.…”

Section: Are the Variations In The Pathways Activated From Step To Stmentioning

confidence: 99%

Training locomotor networks

Edgerton

Courtine

Gerasimenko

et al. 2008

Brain Research Reviews

269

205

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For a complete adult spinal rat to regain some weight-bearing stepping capability, it appears that a sequence of specific proprioceptive inputs that are similar, but not identical, from step to step must be generated over repetitive step cycles. Furthermore, these cycles must include the activation of specific neural circuits that are intrinsic to the lumbosacral spinal cord segments. For these sensorimotor pathways to be effective in generating stepping, the spinal circuitry must be modulated to an appropriate excitability level. This level of modulation is sustained from supraspinal input in intact, but not spinal, rats. In a series of experiments with complete spinal rats, we have shown that an appropriate level of excitability of the spinal circuitry can be achieved using widely different means. For example, this modulation level can be acquired pharmacologically, via epidural electrical stimulation over specific lumbosacral spinal cord segments, and/or by use-dependent mechanisms such as step or stand training. Evidence as to how each of these treatments can "tune" the spinal circuitry to a "physiological state" that enables it to respond appropriately to proprioceptive input will be presented. We have found that each of these interventions can enable the proprioceptive input to actually control extensive details that define the dynamics of stepping over a range of speeds, loads, and directions. A series of experiments will be described that illustrate sensory control of stepping and standing after a spinal cord injury and the necessity for the "physiological state" of the spinal circuitry to be modulated within a critical window of excitability for this control to be manifested. The present findings have important consequences not only for our understanding of how the motor pattern for stepping is formed, but also for the design of rehabilitation intervention to restore lumbosacral circuit function in humans following a spinal cord injury.

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Section: Are the Variations In The Pathways Activated From Step To Stmentioning

confidence: 99%

Training locomotor networks

Edgerton

Courtine

Gerasimenko

et al. 2008

Brain Research Reviews

269

205

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“…In a similar manner, Kalincik et al (30) documented differential regulation of SPNs above vs. below a T4 spinal cord transection. Finally, activity in locomotor circuits is well known to lead to structural plasticity, changes in electrophysiological properties, and altered function within the spinal cord (6,88). Thus altered morphology of SPNs could be associated with their hyperactivity and altered cardiac electrophysiology in spinal cord-injured humans and animals (14).…”

Section: Potential Mechanismsmentioning

confidence: 99%

Structural neuroplasticity following T5 spinal cord transection: increased cardiac sympathetic innervation density and SPN arborization

Lujan

Palani

DiCarlo

2010

American Journal of Physiology-Regulatory, Integrative and Comp

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“…During the last decade, increasing evidence obtained from different spinal cord injury (SCI) models has shown that spinal networks can reorganize spontaneously to contribute to functional recovery [1][2][3][4][5][6][7][8][9] . Adaptive plasticity has as a consequence become an important topic in SCI research.…”

Section: Introductionmentioning

confidence: 99%

A Neonatal Mouse Spinal Cord Compression Injury Model

Züchner

Glover

Boulland

2016

JoVE

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Spinal cord injury (SCI) typically causes devastating neurological deficits, particularly through damage to fibers descending from the brain to the spinal cord. A major current area of research is focused on the mechanisms of adaptive plasticity that underlie spontaneous or induced functional recovery following SCI. Spontaneous functional recovery is reported to be greater early in life, raising interesting questions about how adaptive plasticity changes as the spinal cord develops. To facilitate investigation of this dynamic, we have developed a SCI model in the neonatal mouse. The model has relevance for pediatric SCI, which is too little studied. Because neural plasticity in the adult involves some of the same mechanisms as neural plasticity in early life 1 , this model may potentially have some relevance also for adult SCI. Here we describe the entire procedure for generating a reproducible spinal cord compression (SCC) injury in the neonatal mouse as early as postnatal (P) day 1. SCC is achieved by performing a laminectomy at a given spinal level (here described at thoracic levels 9-11) and then using a modified Yasargil aneurysm mini-clip to rapidly compress and decompress the spinal cord. As previously described, the injured neonatal mice can be tested for behavioral deficits or sacrificed for ex vivo physiological analysis of synaptic connectivity using electrophysiological and high-throughput optical recording techniques 1 . Earlier and ongoing studies using behavioral and physiological assessment have demonstrated a dramatic, acute impairment of hindlimb motility followed by a complete functional recovery within 2 weeks, and the first evidence of changes in functional circuitry at the level of identified descending synaptic connections 1 .

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Plasticity of functional connectivity in the adult spinal cord

Cited by 69 publications

References 72 publications

Training locomotor networks

Training locomotor networks

Structural neuroplasticity following T5 spinal cord transection: increased cardiac sympathetic innervation density and SPN arborization

A Neonatal Mouse Spinal Cord Compression Injury Model

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