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Long‐term induction of c‐jun mRNA and jun protein in rabbit retinal ganglion cells following axotomy or colchicine treatment
Author(s) -
Koistinaho J.,
Hicks K. J.,
Sagar S. M.
Publication year - 1993
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.490340213
Subject(s) - axotomy , colchicine , rabbit (cipher) , microbiology and biotechnology , messenger rna , chemistry , ganglion , retinal ganglion cell , c jun , retinal , biology , neuroscience , regeneration (biology) , medicine , biochemistry , gene , transcription factor , statistics , mathematics
The expression of the c‐jun, c‐fos, and NGFI‐A genes was studied in the rabbit retina after optic nerve crush (ONC) or an intravitreal injection of colchicine. By Northern blotting, the basal expression of c‐fos and NGFI‐A mRNAs were undetectable, whereas c‐jun mRNA showed a low basal expression in shamoperated control retinas. Very few or no Jun‐ or Fosimmunoreactive nuclei were seen in control retinas. From 1 to 95 days after ONC a marked induction of JUN‐ but not FOS‐immunoreactive neurons was seen in the ganglion cell layer peaking at 3 and 7 days. Jun‐positive neurons also accumulated immunoreactive phosphorylated neurofilaments, indicating that they were ganglion cells. Northern blots demonstrated that retinal levels of c‐jun mRNA, but not of c‐fos or NGFI‐A mRNAs, were increased 3 and 7 days after ONC. An intravitreal injection of colchicine also induced Jun‐immunoreactivity within 24 hr in most of the neurons in the ganglion cell layer, but not in the inner nuclear and outer nuclear layers. The results indicate that axonal damage induces a specific pattern of IEG expression including a long‐term induction of the c‐jun gene in CNS neurons. © 1993 Wiley‐Liss, Inc.