Prominent Expression of bFGF in Dorsal Root Ganglia after Axotomy

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 neurons expressed bFGF mRNA in normal DRGs. Nerve injury induced a very dramatic 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 non-neuronal cells. After nerve section, bFGF-LI was in addition found in the cytoplasm, and many more bFGF-positive non-neuronal cells were observed. By means of confocal microscopy analysis of axotomized DRGs, some bFGF-LI could be detected in vesicle-like structures in the cytoplasm as well as in the nucleoli, in addition to the nuclear location. Application of leukaemia inhibitory factor to the transected sciatic nerve significantly increased the number of bFGF-positive neurons, whereas the bFGF-LI in non-neuronal cells was strongly suppressed. About 70% of the normal DRG neurons expressed aFGF mRNA and aFGF-LI. Axotomy produced a moderate increase in aFGF mRNA levels, but no detectable effect on protein levels. Taken together, the results show that bFGF may be involved in the neuronal response to injury and suggest a role in neuronal survival and regeneration in axotomized DRG neurons.

Fibroblast Growth Factor (FGF)-2 and FGF Receptor 3 Are Required for the Development of the Substantia Nigra, and FGF-2 Plays a Crucial Role for the Rescue of Dopaminergic Neurons after 6-Hydroxydopamine Lesion

“…After peripheral nerve injury, FGFR3 was upregulated in contrast to the other FGF-2 receptors (Ji et al, 1995;Grothe and Nikkhah, 2001). Furthermore, this receptor is crucially involved in the regulation of survival of sensory neurons after lesion but not during peripheral nerve development (Jungnickel et al, 2004a(Jungnickel et al, , 2005.…”

Possible role of spinal astrocytes in maintaining chronic pain sensitization: review of current evidence with focus on bFGF/JNK pathway

“…4). An increase in bFGF protein is also evident in DRG neurons after nerve injury (Ji et al, 1995). Although release of bFGF from central terminals of primary sensory neurons after nerve injury has not been shown, bFGF immunoreactivity is present in vesicle-like structures in the cytoplasm, which indicates the possibility that bFGF is released after nerve injury (Ji et al, 1995).…”

“…Scale bar, 25 μm. Reproduced, with permission, from (Ji et al, 1995). Either bFGF or saline was infused intrathecally via an osmotic pump (10 ng μl −1 h −1 ) for one week.…”

Sensing nerve injury at the axonal ER: Activated Luman/CREB3 serves as a novel axonally synthesized retrograde regeneration signal

“…dorsal root ganglion | transcription factor | axotomy | sensory neuron A complex series of cellular and molecular events participates in reprogramming sensory neurons as they transition to a regenerating state following peripheral nerve injury (1)(2)(3)(4)(5)(6)(7). Injury discharge and rapid ion fluxes initiate this transition, followed by the loss of target-derived signals and receipt of retrograde signals from the site of injury (8)(9)(10).…”