Genesis, Neurotrophin Responsiveness, and Apoptosis of a Pronounced Direct Connection between the Two Eyes of the Chick Embryo: A Natural Error or a Meaningful Developmental Event?

Abstract

Unilateral intraocular injections of either of two fluorescent carbocyanine dyes into the embryonic chick eye resulted in both retrograde staining of ganglion cells (GCs) in the eye contralateral to site of injection and anterograde labeling of axons whose cell bodies were located within the injected eye. This prominent retino-retinal projection formed by thousands of GCs having a nasal origin and temporal termination appeared at embryonic day 6 (E6), attained its maximum intensity at E13-E14, and gradually disappeared until E18. The axonal growth cones ended superficially and never penetrated deeper layers of the retina. Treatment of the projection with BDNF resulted in massive terminal branching of the axons within deeper layers of the target retina. Double injection into the eye and the isthmo-optic nucleus showed a concomitant ingrowth of axons in the contralateral retina. Individual GCs died between E9 and E13, but massive apoptotic cell death was mainly monitored at E14 and later. Disintegrated cells showed typical images of apoptosis. Because degenerating cells were prelabeled with the membranophilic fluorescent carbocyanine dye, their death allowed the concomitant visualization of phagocytosing cells, too. Radial Mü ller glia were the only class of cells observed to become phagocytotic between E9 and E16. These cells became replaced exclusively with microglial cells from E17 on. The results suggest that the topologically restricted retinoretinal projection may have some developmental significance rather than representing a massive erroneous projection. Most likely, the projection may serve as a "template" to guide centrifugal isthmo-optic axons into the retina.

Development of microglia in the chick embryo spinal cord: Implications in the regulation of motoneuronal survival and death

“…From BrdU experiments, it is clear that neuronal injury determines active microglial proliferation, in a similar way that has been observed in ricin-induced MN degeneration . Because a proportion of LMC apoptosis does not appear to involve microglial engulfment, other cells such as radial glia may participate in the phagocytosis of apoptotic bodies (Thanos, 1999). We have observed apoptotic bodies within the LMC in close contact with vimentin-labeled radial glia (unpublished results).…”

Distribution of scotoma pattern related to chiasmal lesions with special reference to anterior junction syndrome

“…[21,23]. There is common agreement that the architecture of the prospective chiasm formation [33] and the molecular decoration of the precursor neuroglial cells [1] around the midline account for erroneous fibre pathways such as transient projection of axons into the contralateral optic nerve and retina [43,51]. However, no similar studies have been reported in primates.…”

Ultrastructure of retinal ganglion cell death after axotomy in chick embryos

“…In chick embryos, Mü ller cells are known to phagocytose retinal ganglion cells dying after the administration of concanavalin A (Meller, 1981) and spontaneously degenerating retinoretinal RGCs (Thanos, 1999). However, in quail embryos, the majority of naturally degenerating RGCs are eliminated by microglia (Marin-Teva et al, 1999), and the phagocytic role of microglia in response to degeneration is, of course, well known (Cuadros et al, 2000).…”