Differential proteoglycan expression in two spinal cord regions after dorsal root injury

2009 ◽  
Vol 42 (4) ◽  
pp. 315-327 ◽  
Author(s):  
Laurent Waselle ◽  
Xavier Quaglia ◽  
Anne D. Zurn
Keyword(s):  
Spinal Cord ◽  
Dorsal Root ◽  
Root Injury ◽  
Spinal Cord Regions

scholarly journals Dorsal Root Injury—A Model for Exploring Pathophysiology and Therapeutic Strategies in Spinal Cord Injury

Cells ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 2185
Author(s):  
Håkan Aldskogius ◽  
Elena N. Kozlova
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Dorsal Root ◽  
Molecular Mechanisms ◽  
Dorsal Root Ganglion Neurons ◽  
Descending Pathways ◽  
In Vivo Models ◽  
Root Injury ◽  
Cord Injury ◽  
Ganglion Neurons

Unraveling the cellular and molecular mechanisms of spinal cord injury is fundamental for our possibility to develop successful therapeutic approaches. These approaches need to address the issues of the emergence of a non-permissive environment for axonal growth in the spinal cord, in combination with a failure of injured neurons to mount an effective regeneration program. Experimental in vivo models are of critical importance for exploring the potential clinical relevance of mechanistic findings and therapeutic innovations. However, the highly complex organization of the spinal cord, comprising multiple types of neurons, which form local neural networks, as well as short and long-ranging ascending or descending pathways, complicates detailed dissection of mechanistic processes, as well as identification/verification of therapeutic targets. Inducing different types of dorsal root injury at specific proximo-distal locations provide opportunities to distinguish key components underlying spinal cord regeneration failure. Crushing or cutting the dorsal root allows detailed analysis of the regeneration program of the sensory neurons, as well as of the glial response at the dorsal root-spinal cord interface without direct trauma to the spinal cord. At the same time, a lesion at this interface creates a localized injury of the spinal cord itself, but with an initial neuronal injury affecting only the axons of dorsal root ganglion neurons, and still a glial cell response closely resembling the one seen after direct spinal cord injury. In this review, we provide examples of previous research on dorsal root injury models and how these models can help future exploration of mechanisms and potential therapies for spinal cord injury repair.

Somatotopic organization in cat spinal cord segments with fused dorsal horns: caudal and thoracic levels

1985 ◽  
Vol 54 (5) ◽  
pp. 1167-1177 ◽  
Author(s):  
L. A. Ritz ◽  
J. L. Culberson ◽  
P. B. Brown
Keyword(s):  
Spinal Cord ◽  
Dorsal Horn ◽  
Dorsal Root ◽  
Receptive Fields ◽  
Vertical Orientation ◽  
Dorsal Roots ◽  
Somatotopic Organization ◽  
Dorsal Horns ◽  
Spinal Cord Regions ◽  
Low Threshold

We have explored the somatotopic organization of the two cat spinal cord regions where the dorsal horns are fused (i.e., continuous across the midline): the caudal and thoracic segments. We have mapped the low-threshold component of dorsal horn cell receptive fields (RFs) in these segments and have charted the locations of dorsal root low-threshold mechanoreceptive dermatomes. We also have determined the projections of caudal and thoracic dorsal roots to laminae III and IV by using degeneration techniques. The dorsal skin of the tail or thorax is represented laterally, and ventral skin is represented at the midline, in the fused dorsal horns. Many caudal and thoracic dorsal horn units had RFs that crossed the dorsal or ventral midline of the skin; these units were encountered near the edges or the midline, respectively, of the fused dorsal horns. The tail is fully represented within dorsal root dermatomes S3 to Ca5. Roots more caudal than Ca5 represent progressively smaller skin areas of the distal tail. Adjacent dermatomes overlapped 15-65%. Thoracic dermatomes had a nearly vertical orientation; adjacent dermatomes overlapped by 30-75%. Dorsal roots in caudal and thoracic regions have crossed projections to the medial and lateral (but not middle) portions of the contralateral dorsal horn. These crossed projections are a possible anatomical substrate for RFs that cross the ventral or dorsal midline. The dorsal root projection patterns are consistent with those that would be predicted from the dorsal root dermatomes and dorsal horn cell somatotopy, assuming that the presynaptic terminals' somatotopy is in register with that of dorsal horn cells (the presynaptic somatotopy hypothesis; see Ref. 12).

scholarly journals Profiling sensory neuron microenvironment after peripheral and central axon injury reveals key pathways for neural repair

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Oshri Avraham ◽  
Rui Feng ◽  
Eric Edward Ewan ◽  
Justin Rustenhoven ◽  
Guoyan Zhao ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Peripheral Nerve ◽  
Nerve Injury ◽  
Peripheral Nerve Injury ◽  
Dorsal Root ◽  
Axon Regeneration ◽  
Cell Type ◽  
Root Injury ◽  
Cord Injury

Sensory neurons with cell bodies in dorsal root ganglia (DRG) represent a useful model to study axon regeneration. Whereas regeneration and functional recovery occurs after peripheral nerve injury, spinal cord injury or dorsal root injury is not followed by regenerative outcomes. Regeneration of sensory axons in peripheral nerves is not entirely cell autonomous. Whether the DRG microenvironment influences the different regenerative capacities after injury to peripheral or central axons remains largely unknown. To answer this question, we performed a single-cell transcriptional profiling of mouse DRG in response to peripheral (sciatic nerve crush) and central axon injuries (dorsal root crush and spinal cord injury). Each cell type responded differently to the three types of injuries. All injuries increased the proportion of a cell type that shares features of both immune cells and glial cells. A distinct subset of satellite glial cells (SGC) appeared specifically in response to peripheral nerve injury. Activation of the PPARα signaling pathway in SGC, which promotes axon regeneration after peripheral nerve injury, failed to occur after central axon injuries. Treatment with the FDA-approved PPARα agonist fenofibrate increased axon regeneration after dorsal root injury. This study provides a map of the distinct DRG microenvironment responses to peripheral and central injuries at the single-cell level and highlights that manipulating non-neuronal cells could lead to avenues to promote functional recovery after CNS injuries or disease.

Neurotrophin 3 Improves Delayed Reconstruction of Sensory Pathways After Cervical Dorsal Root Injury

Neurosurgery ◽  
2011 ◽  
Vol 68 (2) ◽  
pp. 450-461 ◽  
Author(s):  
Song Liu ◽  
Stephane Blanchard ◽  
Stephanie Bigou ◽  
Sandrine Vitry ◽  
Delphine Bohl ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Dorsal Root ◽  
Nerve Graft ◽  
Dorsal Root Ganglion Neurons ◽  
Adult Rats ◽  
Sensory Pathways ◽  
Sensory Axons ◽  
Neurotrophin 3 ◽  
Root Injury ◽  
Ganglion Neurons

Abstract BACKGROUND: Spinal root avulsion, or section, results in devastating functional sequels. Whereas reconstruction of motor pathways based on neurotization can reduce motor deficit, associated permanent limb anesthesia limits expected benefit. Sensory pathway reconstruction after dorsal root injury is limited by the inability of re-growing central sensory axons to enter the spinal cord through an injured root. OBJECTIVE: To provide evidence for the reconnection of C7 DRG neurons with the central nervous system (CNS) after experimental section of the C7 dorsal root in adult rats. METHODS: We assessed a new reconstruction strategy in adult rats 9 weeks after transection of C6 and C7 dorsal roots. Re-growing C7 central sensory axons were redirected to the noninjured C5 dorsal root through a nerve graft by end-to-side anastomosis that did not alter the C5 conduction properties. In a subgroup of rats, surgical reconstruction was combined with lentivirus-mediated gene transfer to the nerve graft in order to overexpress neurotrophin 3 (NT-3), a neurotrophic factor that stimulates sensory axon regeneration. RESULTS: Four months after reconstruction, recording of sensory evoked potentials and fluorescent tracer transport showed electrical and physical reconnection of the C7 dorsal root ganglion neurons to the spinal cord through the reconstructed pathway. Sensory perception recovery predominated on proprioception. Axonal regrowth and perception were improved when the nerve graft overexpressed neurotrophin-3 at the time of transplantation. Neurotrophin-3 overexpression did not persist 4 months after transplantation. CONCLUSION: Efficient and functional reconnection of dorsal root ganglion neurons to the spinal cord can be achieved in rats several weeks after cervical dorsal root injury. Surgical repair of sensory pathways could be considered in combination with motor nerve neurotization to treat persisting severe upper limb disability in humans.

scholarly journals Profiling sensory neuron microenvironment after peripheral and central axon injury reveals key pathways for axon regeneration

2020 ◽  
Author(s):  
Oshri Avraham ◽  
Rui Feng ◽  
Eric E. Ewan ◽  
Guoyan Zhao ◽  
Valeria Cavalli
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Single Cell ◽  
Nerve Injury ◽  
Sensory Neurons ◽  
Functional Recovery ◽  
Dorsal Root ◽  
Axon Regeneration ◽  
Root Injury ◽  
Cord Injury

AbstractSensory neurons with cell bodies in dorsal root ganglia (DRG) represent a useful model to study axon regeneration. Whereas regeneration and functional recovery occurs after peripheral nerve injury, spinal cord injury or dorsal root injury is not followed by regenerative outcomes. This results in part from a failure of central injury to elicit a pro-regenerative response in sensory neurons. However, regeneration of sensory axons in peripheral nerves is not entirely cell autonomous. Whether the different regenerative capacities after peripheral or central injury result in part from a lack of response of macrophages, satellite glial cells (SGC) or other non-neuronal cells in the DRG microenvironment remains largely unknown. To answer this question, we performed a single cell transcriptional profiling of DRG in response to peripheral (sciatic nerve crush) and central injuries (dorsal root crush and spinal cord injury). Each cell type responded differently to peripheral and central injuries. Activation of the PPAR signaling pathway in SGC, which promotes axon regeneration after nerve injury, did not occur after central injuries. Treatment with the FDA-approved PPARα agonist fenofibrate, increased axon regeneration after dorsal root injury. This study provides a map of the distinct DRG microenvironment responses to peripheral and central injuries at the single cell level and highlights that manipulating non-neuronal cells could lead to avenues to promote functional recovery after CNS injuries.

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