When optic fibers first approach the chiasmatic region of the diencephalon in the chick embryo on days 3 and 4 (E3-4), they rarely grow rostrally into the olfactory region of the telencephalon. Conversely, olfactory tract axons grow as far as, but never cross the diencephalic/telencephalic (D/T) boundary to enter the optic chiasm. In this study, a region of specialized neuroepithelium, originally named the "knot" in mouse by Silver (1984), has been identified at the D/T border of chick embryos. At pre-axonal stages, the presumptive knot region undergoes a cataclysmic cell death, with concomitant phagocytosis of necrotic debris by the remaining cells. When fibers subsequently appear in the chiasm and olfactory tracts, the knot consists of a very dense, interwoven cluster of non-neuronal cells that lack marginal radial processes, and whose cell bodies directly abut the glial limiting membrane. Thus, the morphology of the knot is in sharp contrast to the cell body-free marginal zone and endfoot regions along which axons tend to grow. In addition, we found that the neural cell adhesion molecule (N-CAM), which is expressed on neuroepithelial cell processes within the central optic and olfactory pathways, is not present on cells in the knot region during periods of axon growth. These results suggest that the knot, through its elimination of the marginal zone processes, absence of large extracellular spaces, and relative absence of adhesion molecules, functions as an axon-refractory barrier that effectively separates the optic and olfactory projections.

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Retinal fibers approach close to the tectal midline but do not encroach on the other side. Just before the entry of retinal axons into the superior colliculus (SC), a group of radial glia differentiates at the tectal midline; the spatiotemporal deployment of these cells points to their involvement in the unilateral containment of retinotectal axons. To test for such a barrier function of the tectal midline cells, we used two lesion paradigms for disrupting their radial processes in the neonatal hamster: (1) a heat lesion was used to destroy the superficial layers of the right SC, including the midline region, and (2) a horizontally oriented hooked wire was inserted from the lateral edge of the left SC toward the midline and was used to undercut the midline cells, leaving intact the retinorecipient layers in the right SC. In both cases, the left SC was denervated by removing its contralateral retinal input. Animals were killed 12 hr to 2 weeks later, after intraocular injections of anterograde tracers to label the axons from the remaining eye. Both lesions resulted in degeneration of the distal processes of the tectal raphe glia and in an abnormal crossing of the tectal midline by retinal axons, leading to an innervation of the opposite ("wrong") tectum. The crossover occurred only where glial cell attachments were disrupted. These results document that during normal development, the integrity of the midline septum is critical in compartmentalizing retinal axons and in retaining the laterality of the retinotectal projection.

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The cellular localizations of the synthetic [3-hydroxyanthranilic acid oxygenase (3HAO)] and degradative [quinolinic acid phosphoribosyltransferase (QPRT)] enzymes of the endogenous excitotoxin quinolinic acid were studied in the adult rat main olfactory bulb by immunohistochemical techniques. 3HAO and QPRT were expressed only in astrocytes. The two enzymes were differentially expressed by astrocytes in a complementary pattern: 3HAO staining was strongest at the glomerular-external plexiform layer junction; QPRT staining was strongest at the glomerular-olfactory nerve layer junction. The complementary distributions of these metabolic enzymes suggests that there could be a gradient of quinolinic acid across the glomerular layer of the main olfactory bulb. Such a gradient could function to restrict the ingrowth of new olfactory axons to the glomeruli and/or to stabilize the formation of new synapses.