Effect of spinal cord injury on neural encoding of spontaneous postural perturbations in the hindlimb sensorimotor cortex

2021 ◽  
Author(s):  
Jaimie Dougherty ◽  
Gregory Disse ◽  
Nathaniel Bridges ◽  
Karen A Moxon
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Sensorimotor Cortex ◽  
Cortical Neurons ◽  
Response To Therapy ◽  
Trunk Muscles ◽  
Ground Reaction Forces ◽  
Cord Injury ◽  
Reaction Forces ◽  
Postural Perturbations

Supraspinal signals play a significant role in compensatory responses to postural perturbations. While the cortex is not necessary for basic postural tasks in intact animals, its role in responding to unexpected postural perturbations after spinal cord injury (SCI) has not been studied. To better understand how SCI impacts cortical encoding of postural perturbations, the activity of single neurons in the hindlimb sensorimotor cortex (HLSMC) was recorded in the rat during unexpected tilts before and after a complete midthoracic spinal transection. In a subset of animals, limb ground reaction forces were also collected. HLSMC activity was strongly modulated in response to different tilt profiles. As the velocity of the tilt increased, more information was conveyed by the HLSMC neurons about the perturbation due to increases in both the number of recruited neurons and the magnitude of their responses. SCI led to attenuated and delayed hindlimb ground reaction forces. However, HLSMC neurons remained responsive to tilts after injury but with increased latencies and decreased tuning to slower tilts. Information conveyed by cortical neurons about the tilts was therefore reduced after SCI, requiring more cells to convey the same amount of information as before the transection. Given that reorganization of the hindlimb sensorimotor cortex in response to therapy after complete mid-thoracic SCI is necessary for behavioral recovery, this sustained encoding of information after SCI could be a substrate for the reorganization that uses sensory information from above the lesion to control trunk muscles that permit weight-supported stepping and postural control.

scholarly journals Autophagy induction stabilizes microtubules and promotes axon regeneration after spinal cord injury

2016 ◽  
Vol 113 (40) ◽  
pp. 11324-11329 ◽  
Author(s):  
Miao He ◽  
Yuetong Ding ◽  
Chen Chu ◽  
Jing Tang ◽  
Qi Xiao ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Cortical Neurons ◽  
Axon Regeneration ◽  
Neuronal Degeneration ◽  
Dorsal Column ◽  
Microtubule Assembly ◽  
Autophagy Induction ◽  
Cord Injury

Remodeling of cytoskeleton structures, such as microtubule assembly, is believed to be crucial for growth cone initiation and regrowth of injured axons. Autophagy plays important roles in maintaining cellular homoeostasis, and its dysfunction causes neuronal degeneration. The role of autophagy in axon regeneration after injury remains speculative. Here we demonstrate a role of autophagy in regulating microtubule dynamics and axon regeneration. We found that autophagy induction promoted neurite outgrowth, attenuated the inhibitory effects of nonpermissive substrate myelin, and decreased the formation of retraction bulbs following axonal injury in cultured cortical neurons. Interestingly, autophagy induction stabilized microtubules by degrading SCG10, a microtubule disassembly protein in neurons. In mice with spinal cord injury, local administration of a specific autophagy-inducing peptide, Tat-beclin1, to lesion sites markedly attenuated axonal retraction of spinal dorsal column axons and cortical spinal tract and promoted regeneration of descending axons following long-term observation. Finally, administration of Tat-beclin1 improved the recovery of motor behaviors of injured mice. These results show a promising effect of an autophagy-inducing reagent on injured axons, providing direct evidence supporting a beneficial role of autophagy in axon regeneration.

scholarly journals Heterogeneous Spine Loss in Layer 5 Cortical Neurons after Spinal Cord Injury

2011 ◽  
Vol 22 (6) ◽  
pp. 1309-1317 ◽  
Author(s):  
A. Ghosh ◽  
S. Peduzzi ◽  
M. Snyder ◽  
R. Schneider ◽  
M. Starkey ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Cortical Neurons ◽  
Cord Injury

scholarly journals Finger somatotopy is preserved after tetraplegia but deteriorates over time

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Sanne Kikkert ◽  
Dario Pfyffer ◽  
Michaela Verling ◽  
Patrick Freund ◽  
Nicole Wenderoth
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Observational Study ◽  
Sensorimotor Cortex ◽  
Structural Mri ◽  
Finger Movement ◽  
Functional Connections ◽  
Cord Injury ◽  
Primary Sensorimotor Cortex ◽  
Over Time

Previous studies showed reorganised and/or altered activity in the primary sensorimotor cortex after a spinal cord injury (SCI), suggested to reflect abnormal processing. However, little is known about whether somatotopically-specific representations can be activated despite reduced or absent afferent hand inputs. In this observational study we used functional MRI and an (attempted) finger movement task in tetraplegic patients to characterise the somatotopic hand layout in primary somatosensory cortex. We further used structural MRI to assess spared spinal tissue bridges. We found that somatotopic hand representations can be activated through attempted finger movements in absence of sensory and motor hand functioning, and no spared spinal tissue bridges. Such preserved hand somatotopy could be exploited by rehabilitation approaches that aim to establish new hand-brain functional connections after SCI (e.g., neuroprosthetics). However, over years since SCI the hand representation somatotopy deteriorated, suggesting that somatotopic hand representations are more easily targeted within the first years after SCI.

scholarly journals Exosome-Mediated siRNA pool Inhibits Axonal Growth Inhibitor in Cortical Neurons of Spinal Cord Injury in Rats

2020 ◽  
Author(s):  
Qi Liao ◽  
Jiang-Hua Ming ◽  
Ge-Liang Hu
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Cell Proliferation ◽  
Cortical Neurons ◽  
Axon Growth ◽  
Axonal Growth ◽  
Growth Inhibitor ◽  
Protective Role ◽  
Primary Cortical Neurons ◽  
Cord Injury

Abstract Background: As exosomes have been confirmed as a reservoir of siRNAs involved in certain diseases, the current study aims to investigate whether exosomal-siRNA could exert a protective role in spinal cord injury (SCI). Methods and Results: Exosomes in our experiment were isolated from lysosomal membrane-associated protein 2b (Lamp2b) overexpression HEK 293T cells, and purity of exosomes was characterized by the expression of CD9, CD47, and CD63 via western blot. Furthermore, the siRNA pool contains four siRNAs including siRNA-NgR, siRNA-LINGO-1, siRNA-Troy, and siRNA-PTEN was loaded to the exosomes, which indicated a significant role for the siRNA pool in reducing the expression of axon growth inhibitory factors. Upon the completion of loading into exosomes (exo-siRNA pool), the exo-siRNA pool was injected into primary cortical neurons of the SCI model in rats before cell proliferation and Rho expression were determined With the results revealed that purified addition could be applied to future experiments. The exo-siRNA pooled transfection caused downregulation of axon growth suppressors in primary cortical neurons including Nogo receptors (NgR), leucine-rich repeats and immunoglobulin domain-containing protein 1 (LINGO-1), Troy, and phosphatase and tenson homolog (PTEN). Cell proliferation and Rho expression of primary cortical neurons inhibited the expression of axonal growth inhibitors in rats with SCI by transfecting exogenous Sirna. Conclusion: This study confirmed that exosomes derived from Lamp2b overexpression HEK 293T cells facilitated both the recovery of functions and the survival of neurons when being loaded with the siRNA pool.

scholarly journals Rescue of axotomized motor cortical neurons from death by bone marrow derived stromal cells transplantation after spinal cord injury in rodent model

IBRO Reports ◽  
2019 ◽  
Vol 6 ◽  
pp. S555
Author(s):  
Khaviyaa Chandramohan ◽  
Lavanya Venkitasamy ◽  
Kirubhanand Chandrashekaran ◽  
Felicia Mary Michael ◽  
Sankar Venkatachalam
Keyword(s):  
Spinal Cord ◽  
Bone Marrow ◽  
Spinal Cord Injury ◽  
Stromal Cells ◽  
Cortical Neurons ◽  
Rodent Model ◽  
Cord Injury ◽  
Motor Cortical

Assessment of Hindlimb Locomotor Strength in Spinal Cord Transected Rats through Animal-Robot Contact Force

2011 ◽  
Vol 133 (12) ◽  
Author(s):  
Jeff A. Nessler ◽  
Moustafa Moustafa-Bayoumi ◽  
Dalziel Soto ◽  
Jessica Duhon ◽  
Ryan Schmitt
Keyword(s):  
Spinal Cord ◽  
Body Weight ◽  
Weight Bearing ◽  
Contact Forces ◽  
Ground Reaction Forces ◽  
Locomotor Training ◽  
Robotic Device ◽  
Thoracic Spinal Cord ◽  
Cord Injury ◽  
Reaction Forces

Robotic locomotor training devices have gained popularity in recent years, yet little has been reported regarding contact forces experienced by the subject performing automated locomotor training, particularly in animal models of neurological injury. The purpose of this study was to develop a means for acquiring contact forces between a robotic device and a rodent model of spinal cord injury through instrumentation of a robotic gait training device (the rat stepper) with miniature force/torque sensors. Sensors were placed at each interface between the robot arm and animal’s hindlimb and underneath the stepping surface of both hindpaws (four sensors total). Twenty four female, Sprague-Dawley rats received mid-thoracic spinal cord transections as neonates and were included in the study. Of these 24 animals, training began for 18 animals at 21 days of age and continued for four weeks at five min/day, five days/week. The remaining six animals were untrained. Animal-robot contact forces were acquired for trained animals weekly and untrained animals every two weeks while stepping in the robotic device with both 60 and 90% of their body weight supported (BWS). Animals that received training significantly increased the number of weight supported steps over the four week training period. Analysis of raw contact forces revealed significant increases in forward swing and ground reaction forces during this time, and multiple aspects of animal-robot contact forces were significantly correlated with weight bearing stepping. However, when contact forces were normalized to animal body weight, these increasing trends were no longer present. Comparison of trained and untrained animals revealed significant differences in normalized ground reaction forces (both horizontal and vertical) and normalized forward swing force. Finally, both forward swing and ground reaction forces were significantly reduced at 90% BWS when compared to the 60% condition. These results suggest that measurement of animal-robot contact forces using the instrumented rat stepper can provide a sensitive and reliable measure of hindlimb locomotor strength and control of flexor and extensor muscle activity in neurologically impaired animals. Additionally, these measures may be useful as a means to quantify training intensity or dose-related functional outcomes of automated training.

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