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Journal of Neuroscience, Vol 15, 4556-4571, Copyright © 1995 by Society for Neuroscience
Lamina-specific expression of adhesion molecules in developing chick optic tectum
M Yamagata, JP Herman and JR Sanes
Department of Anatomy and Neurobiology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
The optic tectum is the major synaptic target of retinal axons in birds. In
the chick, retinal ganglion cell axons enter the optic tectum through a
superficial lamina (the stratum opticum), extended branches into deeper
laminae, and arborize in specific "retinorecipient" laminae, where they
form synapses. Studies using an organotypic culture system have provided
evidence that the tectum bears a series of distinct, lamina-specific, cell
surface-associated cues that direct these axonal behaviors (Yamagata and
Sanes, 1995). Here, we have used a panel of antibodies to 30 membrane and
matrix components to ask whether known adhesive molecules are distributed
in lamina-specific patterns. Among many spatiotemporal pattern of
expression documented, three were particularly noteworthy: (1) The cell
adhesion molecules NgCAM/L1 and TAG-1/axonin-1 were concentrated in the
stratum opticum. (2) SC1/JC7/DM- GRASP/BEN, N-cadherin, neuropilin,
polysialylated N-CAM, and glycoconjugates recognized by the lectin VVA-B4
were concentrated in retinorecipient laminae. (3) Neurofascin,
tenascin-C/cytotactin, and a matrix molecule defined by the "Sigma"
antibody were present at highest levels in areas that border the
retinorecipient laminae. Some members of each group (NgCAM/L1,
TAG-1/axonin, SC1/JC7, polysialic acid, VVA-B4- receptors, and neurofascin)
appeared on schedule and in lamina- restricted patterns in tecta from
embryos that had been enucleated before retinal axons left the eye. Thus,
molecules in these three categories could provide signals to retinal axons
that promote extension through the stratum opticum, induce arborization or
synaptogenesis in retinorecipient laminae, and prevent sprouting into
adjoining laminae. Interestingly, N-cadherin accumulated in retinorecipient
laminae only following the onset of synapse formation, and failed to
accumulate in enucleated tecta. Immunoelectron microscopy of normal tecta
demonstrated the presence of N-cadherin in the synaptic cleft, suggesting a
role for this molecule in synaptic maintenance.
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