Acellular Spinal Cord Scaffolds Combined with Poly (L-Lactic Acid) / Bisperoxovanadium Microspheres Promote Axon Regeneration and Functional Recovery in Spinal Cord Injured Rats

2018 ◽  
Author(s):  
Jia Liu ◽  
Kai Li ◽  
Ke Huang ◽  
Zhi-Peng Huang ◽  
Yupeng He ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Lactic Acid ◽  
Functional Recovery ◽  
Axon Regeneration ◽  
Spinal Cord Injured

scholarly journals Folic Acid Modulates Matrix Metalloproteinase-2 Expression, Alleviates Neuropathic Pain, and Improves Functional Recovery in Spinal Cord-Injured Rats

2017 ◽  
Vol 24 (2) ◽  
pp. 74-81 ◽  
Author(s):  
Gurwattan S. Miranpuri ◽  
Sivan Vadakkadath Meethal ◽  
Emmanuel Sampene ◽  
Abhishek Chopra ◽  
Seah Buttar ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Neuropathic Pain ◽  
Folic Acid ◽  
Matrix Metalloproteinase ◽  
Functional Recovery ◽  
Matrix Metalloproteinase 2 ◽  
Spinal Cord Injured

scholarly journals Nitrous Oxide Impairs Axon Regeneration after Nervous System Injury in Male Rats

2019 ◽  
Vol 131 (5) ◽  
pp. 1063-1076
Author(s):  
Krista J. Stewart ◽  
Bermans J. Iskandar ◽  
Brenton M. Meier ◽  
Elias B. Rizk ◽  
Nithya Hariharan ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Nervous System ◽  
Nitrous Oxide ◽  
Folic Acid ◽  
Functional Recovery ◽  
Axon Regeneration ◽  
Retinal Ganglion ◽  
Cord Injury

Abstract Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New Background Nitrous oxide can induce neurotoxicity. The authors hypothesized that exposure to nitrous oxide impairs axonal regeneration and functional recovery after central nervous system injury. Methods The consequences of single and serial in vivo nitrous oxide exposures on axon regeneration in four experimental male rat models of nervous system injury were measured: in vitro axon regeneration in cell culture after in vivo nitrous oxide administration, in vivo axon regeneration after sharp spinal cord injury, in vivo axon regeneration after sharp optic nerve injury, and in vivo functional recovery after blunt contusion spinal cord injury. Results In vitro axon regeneration 48 h after a single in vivo 70% N2O exposure is less than half that in the absence of nitrous oxide (mean ± SD, 478 ± 275 um; n = 48) versus 210 ± 152 um (n = 48; P < 0.0001). A single exposure to 80% N2O inhibits the beneficial effects of folic acid on in vivo axonal regeneration after sharp spinal cord injury (13.4 ± 7.1% regenerating neurons [n = 12] vs. 0.6 ± 0.7% regenerating neurons [n = 4], P = 0.004). Serial 80% N2O administration reverses the benefit of folic acid on in vivo retinal ganglion cell axon regeneration after sharp optic nerve injury (1277 ± 180 regenerating retinal ganglion cells [n = 7] vs. 895 ± 164 regenerating retinal ganglion cells [n = 7], P = 0.005). Serial 80% N2O exposures reverses the benefit of folic acid on in vivo functional recovery after blunt spinal cord contusion (estimate for fixed effects ± standard error of the estimate: folic acid 5.60 ± 0.54 [n = 9] vs. folic acid + 80% N2O 5.19 ± 0.62 [n = 7], P < 0.0001). Conclusions These data indicate that nitrous oxide can impair the ability of central nervous system neurons to regenerate axons after sharp and blunt trauma.

scholarly journals Nogo-66 Receptor Prevents Raphespinal and Rubrospinal Axon Regeneration and Limits Functional Recovery from Spinal Cord Injury

Neuron ◽  
2004 ◽  
Vol 44 (3) ◽  
pp. 439-451 ◽  
Author(s):  
Ji-Eun Kim ◽  
Betty P. Liu ◽  
James H. Park ◽  
Stephen M. Strittmatter
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Functional Recovery ◽  
Axon Regeneration ◽  
Cord Injury

scholarly journals Assessment of Nogo-66 Receptor 1 Function In Vivo After Spinal Cord Injury

Neurosurgery ◽  
2014 ◽  
Vol 75 (1) ◽  
pp. 51-60 ◽  
Author(s):  
Jing Tong ◽  
Yi Ren ◽  
Xiaowei Wang ◽  
Vassilios G. Dimopoulos ◽  
Henry N. Kesler ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Matrix Metalloproteinase ◽  
Functional Recovery ◽  
Axon Regeneration ◽  
Matrix Metalloproteinase 9 ◽  
Mutant Mice ◽  
Locomotor Function ◽  
Cord Injury ◽  
Metalloproteinase 9

Abstract BACKGROUND: Neuronal Nogo-66 receptor 1 (NgR1) has attracted attention as a converging point for mediating the effects of myelin-associate inhibitory ligands in the central nervous system, establishing the growth-restrictive environment, and limiting axon regeneration after traumatic injury. OBJECTIVE: To investigate the factors that may be contributing to the discrepancy in the importance of NgR1, which has been undermined by several studies that have shown the lack of substantial axon regeneration after spinal cord injury (SCI) in NgR1-knockout or -knockdown animal models. METHODS: We used mice carrying either a homozygous or heterozygous null mutation in the NgR1 gene and subjected them to either a moderate or severe SCI. RESULTS: Locomotor function assessments revealed that the level of functional recovery is affected by the degree of injury suffered. NgR1 ablation enhanced local collateral sprouting in the mutant mice. Reactive astrocytes and chondroitin sulfate proteoglycans (CSPGs) are upregulated surrounding the injury site. Matrix metalloproteinase-9, which has been shown to degrade CSPGs, was significantly upregulated in the homozygous mutant mice compared with the heterozygous or wild-type mice. However, CSPG levels remained higher in the homozygous compared with the heterozygous mice, suggesting that CSPG-degrading activity of matrix metalloproteinase-9 may require the presence of NgR1. CONCLUSION: Genetic ablation of NgR1 may lead to significant recovery in locomotor function after SCI. The difference in locomotor recovery we observed between the groups that suffered various degrees of injury suggests that injury severity may be a confounding factor in functional recovery after SCI.

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