We have studied the expression of basic fibroblast growth factor 2 (FGF-2) and FGF receptor 1 (FGFR1) in the hypoglossal motor system during degeneration and regeneration by using an RNase protection assay, in situ hybridization, and Western blot analysis. The FGF-2 transcript was found to be weakly expressed in the hypoglossal motoneurons of the adult rat. Both peripheral transection and crush injury of the hypoglossal nerve resulted in a marked up-regulation of the FGF-2 mRNA in motoneurons of the hypoglossal nucleus (with a peak at 10 and 11 days postlesion) as well as in the proximal and distal nerve stumps. The FGFR1 transcript was strongly expressed by hypoglossal motoneurons of unlesioned rats. Neither axotomy nor crush lesion of the hypoglossal nerve revealed any alteration of the expression level and cellular localization in the hypoglossal nucleus, but they did result in a significant increase of the FGFR1 mRNA level in the proximal and distal nerve stump. Western blot analysis of the hypoglossal nucleus revealed the presence of the 21 kD and 23 kD isoforms and of a weak expression of the 18 kD isoform. Hypoglossal nerve transection resulted in a complete down-regulation of the FGF-2 protein 3 days after lesion. After 14 days, however, the level of the three isoforms was increased above the control level. The regulation of FGF-2 in hypoglossal motoneurons after experimental nerve injury is in agreement with the idea of a lesion-related function of FGF-2. Together with previously reported neurotrophic effects, these results suggest that FGF-2 provides trophic support for lesioned motoneurons. At the injury site, FGF-2 could be involved in the regulation of the myelination.

We have studied the expression of basic fibroblast growth factor 2 (FGF-2) and FGF receptor 1 (FGFR1) in the hypoglossal motor system during degeneration and regeneration by using an RNase protection assay, in situ hybridization, and Western blot analysis. The FGF-2 transcript was found to be weakly expressed in the hypoglossal motoneurons of the adult rat. Both peripheral transection and crush injury of the hypoglossal nerve resulted in a marked up-regulation of the FGF-2 mRNA in motoneurons of the hypoglossal nucleus (with a peak at 10 and 11 days postlesion) as well as in the proximal and distal nerve stumps. The FGFR1 transcript was strongly expressed by hypoglossal motoneurons of unlesioned rats. Neither axotomy nor crush lesion of the hypoglossal nerve revealed any alteration of the expression level and cellular localization in the hypoglossal nucleus, but they did result in a significant increase of the FGFR1 mRNA level in the proximal and distal nerve stump. Western blot analysis of the hypoglossal nucleus revealed the presence of the 21 kD and 23 kD isoforms and of a weak expression of the 18 kD isoform. Hypoglossal nerve transection resulted in a complete down-regulation of the FGF-2 protein 3 days after lesion. After 14 days, however, the level of the three isoforms was increased above the control level. The regulation of FGF-2 in hypoglossal motoneurons after experimental nerve injury is in agreement with the idea of a lesion-related function of FGF-2. Together with previously reported neurotrophic effects, these results suggest that FGF-2 provides trophic support for lesioned motoneurons. At the injury site, FGF-2 could be involved in the regulation of the myelination.