In response to peripheral nerve lesion, synthesis of basic fibroblast growth factor (FGF-2) increases in sensory ganglia and motoneurons. Here, we investigated the axotomy-induced regulation of FGF-2 and FGF receptor-1 (FGFR-1) expression in the autonomic nervous system using the sympathetic superior cervical ganglion of the adult rat as a model. Transcripts for both proteins were detected by ribonuclease protection assay. Western blotting indicated the presence of all three FGF-2 isoforms (18, 21, and 23 kD) in the superior cervical ganglion. Immunohistochemical analysis revealed FGF-2 localization in nuclei of satellite cells surrounding postganglionic perikarya. After transection of the carotid nerves, the number of FGF-2-immunoreactive glial cells increased. FGF-2 mRNA was up-regulated within 6 h and remained elevated for 3 weeks. The 18-, 21-, and 23-kD isoforms were all increased 7 days after axotomy. FGFR-1 immunoreactivity was observed in neuronal and nonneuronal nuclei in the normal rat superior cervical ganglion. In contrast to FGF-2, expression of FGFR-1 was unchanged in ganglia after axotomy. Taken together, the present results suggest that FGF-2 participates in neuron-glial interactions of sympathetic ganglia and may be involved in sympathetic neuron survival or nerve regeneration after nerve lesion.
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Klimaschewski et al. (1999) studied this question.
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