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Neuronal and glial expression of the adhesion molecule TAG‐1 is regulated after peripheral nerve lesion or central neurodegeneration of adult nervous system
Author(s) -
Soares Sylvia,
Traka Maria,
Von Boxberg Ysander,
Bouquet Céline,
Karagogeos Domna,
Nothias Fatiha
Publication year - 2005
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2005.03961.x
Subject(s) - in situ hybridization , lesion , spinal cord , biology , neuroscience , central nervous system , neurodegeneration , sciatic nerve , spinal cord injury , cell adhesion molecule , neuron , microbiology and biotechnology , pathology , anatomy , gene expression , medicine , biochemistry , disease , gene
Expression of the cell adhesion molecule TAG‐1 is down‐regulated in adult brain, with the exception of certain areas exhibiting structural plasticity. Here, we present evidence that TAG‐1 expression persists also in adult rat spinal cord and dorsal root ganglia (DRG), and can be up‐regulated after injury. On Western blots of adult tissue, TAG‐1 is detected as a 135‐kDa band, with an additional specific 90‐kDa band, not present in developing tissue. TAG‐1 expression is found both in DRG neurons and in Schwann cells, particularly those associated with the peripherally projecting DRG processes. Quantitative in situ hybridization revealed that TAG‐1 expression is significantly higher in small neurons that give rise to unmyelinated fibers, than in large DRG neurons. The regulation of TAG‐1 was then examined in two different lesion paradigms. After a sciatic nerve lesion, TAG‐1 expression is not up‐regulated in DRG neurons, but decreases with time. At the lesion site, reactive Schwann cells up‐regulate TAG‐1, as demonstrated by both immunohistochemistry and in situ hybridization. In a second paradigm, we injected kainic acid into the spinal cord that kills neurons but spares glia and axons. TAG‐1 is up‐regulated in the spinal neuron‐depleted area as well as in the corresponding dorsal and ventral roots, associated with both target‐deprived afferent fibers and with the non‐neuronal cells that invade the lesion site. These results demonstrate a local up‐regulation of TAG‐1 in the adult that is induced in response to injury, suggesting its involvement in axonal re‐modelling, neuron–glia interactions, and glial cell migration.