Abstract

Two sorts of glial cell are associated with sympathetic ganglia — Schwann cells, which are associated with peripheral nerves, and sympathetic (satellite) glia, which support neurons in ganglia. The development of sympathetic neurons has been very well studied over many years, but surprisingly little is known about the development of sympathetic glia. We examined the development of sympathetic glia in mouse sympathetic ganglia in both wild type and transgenic mice. Previous studies have shown that brain-derived fatty acid binding protein (B-FABP) is a marker of glial precursors. In wild type mice, B-FABP+cells were first detected immunohistochemically at E11.5. The first BFABP+cells appeared in the most superficial layer of the ganglion, but by E12.5 they were also present deeper in the ganglion, where they continued to increase in number until the adult density and appearance was reached by E16.5. B-FABP was never colocalised with immunoreactivity to tyrosine hydroxylase at any embryonic stage. A marker of mature peripheral glial cells, S100b, did not appear until E15.5. In heterozygote mice in which green fluorescent protein (GFP) expression is driven by the Ret-promoter, B-FABP was never co-localised with GFP. However, sympathetic glial precursors did express high levels of immunoreactivity for GDNF family ligand receptor alpha 1 (GFRalpha1) between E10.5 and E14.5. GDNF-GFRalpha1 can utilise neural cell adhesion molecule (NCAM) rather than Ret as the transmembrane signalling component. NCAM was present in B-FABP immunoreactive cells. An examination of GDNF null mutants suggested that there were no obvious consequences to satellite glial development of the loss of GDNF.

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