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c‐Jun expression after axotomy of corneal trigeminal ganglion neurons is dependent on the site of injury
Author(s) -
De Felipe Carmen,
Belmonte Carlos
Publication year - 1999
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 - 10.1046/j.1460-9568.1999.00498.x
Subject(s) - axotomy , trigeminal ganglion , c jun , regeneration (biology) , biology , neuroscience , population , cornea , calcitonin gene related peptide , sema3a , anatomy , microbiology and biotechnology , sensory system , neuropeptide , medicine , semaphorin , biochemistry , receptor , environmental health , gene , transcription factor
The proto‐oncogene c‐ Jun has been implicated in the control of neuronal responses to injury and in axonal growth during regenerative processes. We have investigated the expression of c‐ Jun during normal terminal remodelling in trigeminal ganglion neurons innervating the cornea and after acute injury of epithelial nerve terminals or parent axons. Remodelling and rearrangement, or damage limited to corneal epithelium endings, was not a trigger for activation of c‐ Jun expression. However, injury of parent axons in the stroma or in the orbital ciliary nerves induced c‐ Jun expression in 50% of the population of corneal neurons, which included all of the large myelinated and 20% of the small neuropeptide‐containing corneal neurons. This suggests that c‐ Jun expression in trigeminal ganglion neurons is not associated with normal remodelling or regeneration of peripheral nerve terminals, and that it takes place only when parent axons are injured. A substantial number of damaged neurons do not express c‐ Jun , indicating that in primary sensory neurons, injury and regeneration may not always be coupled to the expression of this proto‐oncogene.