Perspectives on the treatment of the longitudinal spinal cord injury

Carlstedt, Thomas

doi:10.3389/fneur.2010.00011

Cited by 5 publications

(6 citation statements)

References 30 publications

(41 reference statements)

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“…In a previous communication, the basic science background and its clinical translation to the first surgical method that results in functional return after a spinal cord injury was given (1). The traumatic tear of nerve roots from the spinal cord interrupts the segmental transverse sensory and motor nerve fibers causing a longitudinal spinal cord injury.…”

Section: Introductionmentioning

confidence: 99%

“…Proteoglycan producing NG2 cells have been indicated to participate in such process (11), and it is therefore pertinent to further study these cells in conjunction with dorsal root de- and regeneration across the PNS–CNS transitional region (see below). Since the previous communication (1), experimental and clinical studies have been performed in order to overcome the problem of sensory recovery after dorsal root avulsion injury.…”

Section: Introductionmentioning

confidence: 99%

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New Treatments for Spinal Nerve Root Avulsion Injury

Carlstedt

2016

Front. Neurol.

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Further progress in the treatment of the longitudinal spinal cord injury has been made. In an inverted translational study, it has been demonstrated that return of sensory function can be achieved by bypassing the avulsed dorsal root ganglion neurons. Dendritic growth from spinal cord sensory neurons could replace dorsal root ganglion axons and re-establish a reflex arch. Another research avenue has led to the development of adjuvant therapy for regeneration following dorsal root to spinal cord implantation in root avulsion injury. A small, lipophilic molecule that can be given orally acts on the retinoic acid receptor system as an agonist. Upregulation of dorsal root ganglion regenerative ability and organization of glia reaction to injury were demonstrated in treated animals. The dual effect of this substance may open new avenues for the treatment of root avulsion and spinal cord injuries.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

New Treatments for Spinal Nerve Root Avulsion Injury

Carlstedt

2016

Front. Neurol.

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“…Increased survival of MN after replantation of an avulsed ventral root has also been described recently (Eggers et al, 2010). In humans, replantation of an avulsed ventral root after traumatic root avulsions has even been shown to be functional (Carlstedt et al, 1995). In order to further increase survival of MN after root avulsion, neurotrophins has also been added locally after replantation of the avulsed root into the spinal cord (Blits et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

Activating Transcription Factor 3, a Useful Marker for Regenerative Response after Nerve Root Injury

2011

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Activating transcription factor 3 (ATF3) is induced in various tissues in response to stress. In this experiment, ATF3 expression was studied in adult rats subjected either to a dorsal or ventral root avulsion (VRA; L4-6), or sciatic nerve transection (SNT). Post-operative survival times varied between 1.5 h and 3 weeks. In additional experiments an avulsed ventral root was directly replanted to the spinal cord. Dorsal root ganglias (DRGs) from humans exposed to traumatic dorsal root avulsions were also examined. After SNT ATF3 immunoreactivity (ATF3 IR) was detected in a few DRG neurons already 6 h after the lesion. After 24 h the number had clearly increased and still at 3 weeks DRG neurons remained labeled. In the ventral horn, ATF3 IR in motoneurons (MN) was first detected 24 h after the SNT, and still 3 weeks post-operatively lesioned MN showed ATF3 labeling. After a VRA many spinal MN showed ATF3 IR already after 3 h, and after 6 h all MN were labeled. At 3 weeks a majority of the lesioned MN had died, but all the remaining ones were labeled. When an avulsed ventral root was directly replanted, MN survived and were still labeled at 5 weeks. In DRG, a few neurons were labeled already at 1.5 h after a dorsal root avulsion. At 24 h the number had increased but still only a minority of the neurons were labeled. At 3 days the number of labeled neurons was reduced, and a further reduction was at hand at 7 days and 3 weeks. In parallel, in humans, 3 days after a traumatic dorsal root avulsion, only a few DRG neurons showed ATF3 IR. At 6 weeks no labeled neurons could be detected. These facts imply that ATF3 response to axotomy involves a distance-dependent mechanism. ATF3 also appears to be a useful and reliable neuronal marker of nerve lesions even in humans. In addition, ATF3 up-regulation in both motor and sensory neurons seems to be linked to regenerative competence.

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“…Potential therapies to promote axon regrowth and functional recovery have been considered (Duraikannu, Krishnan, Chandrasekhar, & Zochodne, 2019;Havton & Carlstedt, 2009). Yet, the limits of current treatments outline the need for further basic research into mechanisms that enhance motor axon regeneration (Carlstedt, 2010).…”

Section: Introductionmentioning

confidence: 99%

Regeneration of spinal motor axons: Negative regulation by Celsr2 implicating Cdc42/Rac1 and JNK/c-Jun signaling

Wen

Weng

Liu

et al. 2021

Preprint

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During development, cadherins Celsr2 and Celsr3 control axon navigation. Unlike Celsr3, Celsr2 remains expressed in the adult, suggesting unexplored roles in maintenance and repair. Here we show that Celsr2 knockdown promotes motor axon regeneration in mouse and human spinal cord explants and cultured motor neurons. Celsr2 downregulation is accompanied by increased levels of GTP-bound Rac1 and Cdc42, and of JNK and c-Jun proteins. Using a branchial plexus injury model, we show that forelimb functional recovery is improved in Celsr2 mutant versus control mice. Compared to controls, in mutant mice, reinnervated biceps muscles are less atrophic, contain more newly formed neuromuscular junctions, and generate larger electromyographic potentials, while motor neuron survival and axon regeneration are improved. GTP-bound Rac1 and Cdc42, JNK and c-Jun are upregulated in injured mutant versus control spinal cord. In conclusion, Celsr2 negatively regulates motor axon regeneration via Cdc42/Rac1/JNK/c-Jun signaling and is a target for neural repair.

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Perspectives on the treatment of the longitudinal spinal cord injury

Cited by 5 publications

References 30 publications

New Treatments for Spinal Nerve Root Avulsion Injury

New Treatments for Spinal Nerve Root Avulsion Injury

Activating Transcription Factor 3, a Useful Marker for Regenerative Response after Nerve Root Injury

Regeneration of spinal motor axons: Negative regulation by Celsr2 implicating Cdc42/Rac1 and JNK/c-Jun signaling

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