Abstract
The L1 family of cell adhesion molecules (L1-CAMs) is known to be involved in various neuronal functions such as cell adhesion, axon guidance, and synaptic plasticity. We investigated the detailed expression/changes of a close homolog of the L1 cell adhesion molecule (CHL1) after nerve injury and the possible role on neuropathic pain using the rat spared nerve injury (SNI) model. SNI induced the expression of CHL1 in L4/5 DRG neurons, particularly in small-size injured neurons and in satellite cells. In the spinal cord, CHL1 immunoreactivity increased mainly in laminae I-II of the dorsal horn on the side ipsilateral to the nerve injury. Ultrastructural study clarified the fine localization of CHL1 in axons of primary afferents in the dorsal horn. CHL1 immunoreactivities were localized in the adherence such as axon-axon, axon-dorsal horn neurons (dendrite, soma), and axon-glial cells (astrocyte and microglia). Experimental inhibition of CHL1 adhesion by intrathecal administration of the antibody for CHL1 extracellular domain significantly prevented and reversed SNI-induced mechanical allodynia. Thus, alterations of CHL1 may be involved in the structural plasticity after peripheral nerve injury and have important roles in neuropathic pain.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.