The development of radial glia and astrocytes in the telencephalon of the lizard Gallotia galloti was studied by immunohistochemistry with anti-vimentin and anti-GFAP antibodies. Vimentin appears at embryonic stage 32 (E32) in the proliferative zone of the lateral ventricle and subpial end-feet in the marginal zone. At E34-35 the staining intensity for vimentin in all radial glia is maximal. It then decreases and disappears in most structures in adult animals. GFAP appears at E35 in the end-feet in the marginal zone and its intensity increases until adulthood, particularly in radial and sinuous fibers and in fibers that originate from the sulci and invade the ventral striatum and the septum. In contrast, the reaction is weak in the cortex, in the anterior dorso-ventricular ridge, and in the amygdala nuclei. Radial glia is still present in the adult, and the composition of its intermediate filaments changes during development from vimentin to GFAP. No GFA-positive cell bodies except those of ependymal glia were detected in telencephalon.
Using anterograde tracing with HRPand antibodies (ABs) against neurofilaments, we show that regrowth of retinal ganglion cell (RGC) axons in the lizard Gallotia galloti commences only 2 months after optic nerve transection (ONS) and continues over at least 9 months. This is unusually long when compared to RGC axon regeneration in fish or amphibians. Following ONS, lizard RGCs up-regulate the immediate early gene C-JUN for 9 months or longer, indicating their reactive state. In keeping with the in vivo data, axon outgrowth from lizard retinal explants is increased above control levels from 6 weeks, reaches its maximum as late as 3 months, and remains elevated for at least 1 year after ONS. By means of BrdU incorporation assays and antiproliferating cell nuclear antigen immunohistochemistry, we show that the late axon outgrowth is not derived from new RGCs that might have arisen in reaction to ONS: no labeled cells were detected in lizard retinas at 0.5, 1, 1.5, 3, 6, and 12 months after ONS. Conversely, numbers of RGCs undergoing apoptosis were too low to be detectable in TUNEL assays at any time after ONS. These results demonstrate that retinal axon regeneration in G. galloti is due to axon regrowth from the resident population of RGCs, which remain in a reactive state over an extended time interval. Neurogenesis does not appear to be involved in RGC axon regrowth in G. galloti.
The distribution of glial fibrillary acidic protein (GFAP)- and vimentin-containing cells was studied by immunohistochemistry in the midbrain of the lizard Gallotia galloti. At embryonic stage 32 (E32), vimentin immunoreactivity appeared first in cell bodies located in the ventricular walls, in radial fibers, and subpial end-feet and increased in these structures until E34/E35. Faint GFAP immunoreactivity gradually appeared in the same structures between E34 and E37, and this increased until adulthood, whereas vimentin immunoreactivity decreased after E35, becoming limited to a few end-feet and fibers in the adult, mainly in the tegmentum. Thus, in developing Gallotia midbrain a shift from vimentin-containing to GFAP-containing intermediate filaments begins around E36 or E37. At E40, in addition to the cell bodies in the ependymal area, dispersed GFAP-positive cells, possibly immature astrocytes appeared. These cells showed the same shift. In the adult lizard, GFAP-positive radial glia are still present and coexist with GFAP-positive astrocytes, which are prefentially located in the marginal optic tract and the oculomotor nuclei, but are absent in the fasciculus longitudinalis medialis. Optic tectum, pretectum, tegmentum, and isthmic nuclei are the areas richest in GFAP-positive radial fibers: these were much less abundant in the deep mesencephalic nuclei. Thus, in this lizard, GFAP-positive astrocytes display a clear cut regional distribution: they are present in mesencephalon, whereas they are absent in telencephalon.
Retinal ganglion cell (RGC) axons in lizards (reptiles) were found to regenerate after optic nerve injury. To determine whether regeneration occurs because the visual pathway has growth-supporting glia cells or whether RGC axons regrow despite the presence of neurite growth-inhibitory components, the substrate properties of lizard optic nerve myelin and of oligodendrocytes were analyzed in vitro, using rat dorsal root ganglion (DRG) neurons. In addition, the response of lizard RGC axons upon contact with rat and reptilian oligodendrocytes or with myelin proteins from the mammalian central nervous system (CNS) was monitored. Lizard optic nerve myelin inhibited extension of rat DRG neurites, and lizard oligodendrocytes elicited DRG growth cone collapse. Both effects were partially reversed by antibody IN-1 against mammalian 35/250 kD neurite growth inhibitors, and IN-1 stained myelinated fiber tracts in the lizard CNS. However, lizard RGC growth cones grew freely across oligodendrocytes from the rat and the reptilian CNS. Mammalian CNS myelin proteins reconstituted into liposomes and added to elongating lizard RGC axons caused at most a transient collapse reaction. Growth cones always recovered within an hour and regrew.Thus, lizard CNS myelin and oligodendrocytes possess nonpermissive substrate properties for DRG neurons-like corresponding structures and cells in the mammalian CNS, including mammalian-like neurite growth inhibitors. Lizard RGC axons, however, appear to be far less sensitive to these inhibitory substrate components and therefore may be able to regenerate through the visual pathway despite the presence of myelin and oligodendrocytes that block growth of DRG neurites.
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