ArticleThe European journal of neuroscience2007
Alteration of the cell adhesion molecule L1 expression in a specific subset of primary afferent neurons contributes to neuropathic pain.
Article in The European journal of neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- Jun N-terminal kinase's role in neuropathic pain: C-fiber remodeling and growth-associated protein-43 phosphorylation.Pain reports · 2025Article
- RNAcare: integrating clinical data with transcriptomic evidence using rheumatoid arthritis as a case study.BMC medical genomics · 2025Article
- Inherited mitochondrial dysfunction triggered by OPA1 mutation impacts the sensory innervation fibre identity, functionality and regenerative potential in the cornea.Scientific reports · 2024Article
- Nerves in the Tumor Microenvironment: Origin and Effects.Frontiers in cell and developmental biology · 2020Review
- Increased Expression of Fibronectin Leucine-Rich Transmembrane Protein 3 in the Dorsal Root Ganglion Induces Neuropathic Pain in Rats.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- CXCR4/SDF1 signalling promotes sensory neuron clusteringBiology open · 2018Article
- Article
- Synergistic effects of Buyang Huanwu decoction and embryonic neural stem cell transplantation on the recovery of neurological function in a rat model of spinal cord injury.Experimental and therapeutic medicine · 2015Article
- Analysis of human embryonic stem cells with regulatable expression of the cell adhesion molecule l1 in regeneration after spinal cord injury.Journal of neurotrauma · 2014Article
- Functional genomic screen and network analysis reveal novel modifiers of tauopathy dissociated from tau phosphorylation.Human molecular genetics · 2011Article
- L1 cell adhesion molecule is essential for the maintenance of hyperalgesia after spinal cord injury.Experimental neurology · 2009Article
- Persistent changes in spinal cord gene expression after recovery from inflammatory hyperalgesia: a preliminary study on pain memory.BMC neuroscience · 2008Article
- Interaction of transient receptor potential vanilloid 4, integrin, and SRC tyrosine kinase in mechanical hyperalgesia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- Article
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Authors and funding
6 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The cell adhesion molecule L1 (L1-CAM) plays important functional roles in the developing and adult nervous systems. Here we show that peripheral nerve injury induced dynamic post-transcriptional alteration of L1-CAM in the rat dorsal root ganglia (DRGs) and spinal cord. Sciatic nerve transection (SCNT) changed the expression of L1-CAM protein but not L1-CAM mRNA. In DRGs, SCNT induced accumulation of the L1-CAM into the surface of somata, which resulted in the formation of immunoreactive ring structures in a number of unmyelinated C-fiber neurons. These neurons with L1-CAM-immunoreactive ring structures were heavily colocalized with phosphorylated p38 MAPK. Western blot analysis revealed the increase of full-length L1-CAM and decrease of fragments of L1-CAM after SCNT in DRGs. Following SCNT, L1-CAM-immunoreactive profiles in the dorsal horn showed an increase mainly in pre-synaptic areas of laminae I-II with a delayed onset and colocalized with growth-associated protein 43. In contrast to DRGs, SCNT increased the proteolytic 80-kDa fragment of L1-CAM and decreased full-length L1-CAM in the spinal cord. The intrathecal injection of L1-CAM antibody for the extracellular domain of L1-CAM inhibited activation of p38 MAPK and emergence of ring structures of L1-CAM immunoreactivity in injured DRG neurons. Moreover, inhibition of extracellular L1-CAM binding by intrathecal administration of antibody suppressed the mechanical allodynia and thermal hyperalgesia induced by partial SCNT. Collectively, these data suggest that the modification of L1-CAM in nociceptive pathways might be an important pathomechanism of neuropathic pain.
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