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Increase of close homolog of cell adhesion molecule L1 in primary afferent by nerve injury and the contribution to neuropathic pain
Author(s) -
Yamanaka Hiroki,
Kobayashi Kimiko,
Okubo Masamichi,
Fukuoka Tetsuo,
Noguchi Koichi
Publication year - 2011
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.22588
Subject(s) - sni , axon , nerve injury , astrocyte , neural cell adhesion molecule , cell adhesion molecule , biology , neuropathic pain , neuroscience , spinal cord , peripheral nerve injury , microglia , microbiology and biotechnology , central nervous system , cell adhesion , cell , immunology , inflammation , regeneration (biology) , biochemistry , genetics , hydrolysis , acid hydrolysis
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. J. Comp. Neurol. 519:1597–1615, 2011. © 2010 Wiley‐Liss, Inc.