Intraperitoneal injection of the neurotoxin 3-acetylpyridine (3AP) induces
a rapid degeneration of the medial cerebral cortex (lizard fascia dentata)
granular layer and of its zinc enriched axonal projection (lizard mossy fib
res). After 6-8 weeks post-lesion the cell debris have been removed and the
granular layer is repopulated by neurons generated in the subjacent ependy
ma. Both processes, neuron incorporation and debris removal, seem to be cru
cial for successful regeneration. Scavenging processes in the lesioned mamm
alian CNS are usually carried out by microglia and/or astrocytes. In the li
zard cerebral cortex there are no free astrocytes and the only glial fibril
lary acid (GFAP) immunoreactive cells are radial glia-ependymocytes, simila
r to those present during mammalian CNS development. Ependymocytes, in addi
tion to their help in vertical migrations of just generated immature neuron
s, built the cortical glial scaffold, insulate the blood capillaries, form
the outer glial limiting membrane, thus playing an essential role in the li
zard cortical blood-brain barrier. In this study, by means of GFAP-immunocy
tochemistry and electron microscopy, we have shown that radial glial cells
participate actively in the removal/phagocytosis of cellular debris generat
ed in the lesion process: mainly degenerated synapses, but interestingly, a
lso some neuronal somata. Cell debris taken up by ependymocyte lateral proc
esses seem to be progressively transported to either distal (pial) or proxi
mal (ventricular) pores of the cell, where they result in lipofuscin accumu
lations. The hypothetical subsequent exchange of debris from ependymoglia b
y microglia/macrophages and Kolmer cells is discussed.