PROMINENT EXPRESSION OF BFGF IN DORSAL-ROOT GANGLIA AFTER AXOTOMY

Citation
Rr. Ji et al., PROMINENT EXPRESSION OF BFGF IN DORSAL-ROOT GANGLIA AFTER AXOTOMY, European journal of neuroscience, 7(12), 1995, pp. 2458-2468
Citations number
75
Categorie Soggetti
Neurosciences
ISSN journal
0953816X
Volume
7
Issue
12
Year of publication
1995
Pages
2458 - 2468
Database
ISI
SICI code
0953-816X(1995)7:12<2458:PEOBID>2.0.ZU;2-K
Abstract
Using quantitative in situ hybridization and immunohistochemistry the expression of acidic and basic fibroblast growth factors (aFGF, bFGF) in dorsal root ganglia (DRGs) was examined. Around 5% of the small neu rons expressed bFGF mRNA in normal DRGs. Nerve injury induced a very d ramatic and rapid up-regulation in bFGF mRNA levels, and around 80% of all DRG neurons expressed bFGF mRNA 3 days after axotomy. A distinct increase in bFGF-like immunoreactivity (LI) was also detected as early as 15 h after axotomy. The elevation of bFGF mRNA and protein levels declined after 1 week. bFGF mRNA was also up-regulated in non-neuronal cells following axotomy. Normally bFGF-LI was mainly localized in the nuclei of DRG neurons and in some nonneuronal cells. After nerve sect ion, bFGF-LI was in addition found in the cytoplasm, and many more bFG F-positive non-neuronal cells were observed. By means of confocal micr oscopy analysis of axotomized DRGs, some bFGF-LI could be detected in vesicle-like structures in the cytoplasm as well as in the nucleoli, i n addition to the nuclear location. Application of leukaemia inhibitor y factor to the transected sciatic nerve significantly increased the n umber of bFGF-positive neurons, whereas the bFGF-LI in non-neuronal ce lls was strongly suppressed. About 70% of the normal DRG neurons expre ssed aFGF mRNA and aFGF-LI. Axotomy produced a moderate increase in aF GF mRNA levels, but no detectable effect on protein levels. Taken toge ther, the results show that bFGF may be involved in the neuronal respo nse to injury and suggest a role in neuronal survival and regeneration in axotomized DRG neurons.