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Notes: Summary In order to investigate axolemmal development in a glial cell deficient environment, normal and irradiated dorsal funiculus in rat lumbosacral spinal cord was examined by freeze-fracture electron microscopy. At 3 days of age, normal fibres are all unmyelinated and of small (〈0.5 μm) diameter. The unmyelinated axons have a moderate density (∼850 μm−2) of intramembranous particles (IMPs) on P-fracture faces and a low IMP density (∼300 μm−2) on E-faces. IMPs are homogeneously distributed along both fracture faces. By 19 days of age, the normal dorsal funiculus is well populated with myelinated axons and glial cells, as well as a sizable population of unmyelinated fibres. Nearly all of the myelinated fibres have a large (〉1.0 μm) diameter; whereas, most unmyelinated axons are of small (〈0.5 μm) calibre. The axolemma of unmyelinated axons is relatively undifferentiated, with an asymmetrical distribution of IMPs (P-face: ∼1100 μm−2; E-face: ∼450 μm−2). Myelinated fibres show nodal and paranodal regions with P-face and E-face ultrastructure similar to previous descriptions. Internodal axolemma appears relatively homogeneous, with P-faces being highly particulate (∼2100 μm−2) and a low IMP density (∼200 μm−2) on E-faces. Following irradiation of the lumbosacral spinal cord at 3 days of age, there is a severe reduction in the number of glial cells and myelinated fibres in this region when the tissue is examined at 19 days of age. Despite the deficiency of glial cells in this tissue, axonal and axolemmal development continue. Numerous large (〉1.0 μm) diameter axons are present in this irradiated tissue. Large diameter axons show a high (∼2000 μm−2) density of IMPs on P-faces; E-face IMP density remains at ∼440 μm−2. Small calibre axons also have an asymmetrical distribution of particles (P-face: ∼1100 μm−2; E-face: 280 μm−2). The axolemmal E-faces of some glial cell deprived fibres exhibit regions with greater than normal (∼750 μm−2) density of IMPs. These results demonstrate that some aspects of axonal and axolemmal development continue in a glial cell deficient environment, and it is suggested that axolemmal ultrastructure is, at least in part, independent of glial cell association.