Tenascin demarcates the boundary between the myelinated and nonmyelinated part of retinal ganglion cell axons in the developing and adult mouse

Abstract

The molecular determinants controlling the topographically restricted distribution of neural cells in the mammalian CNS are largely unknown. In the mouse, myelin-forming oligodendrocytes are differentially distributed along retinal ganglion cell axons. These axons are myelin free intraretinally and in the most proximal (i.e., retinal) part of the optic nerve, but become myelinated in the distal (i.e., chiasmal) part of the optic nerve. Tenascin protein and mRNA are detectable in increased amounts at the retinal end of the developing optic nerve before the arrival of oligodendrocyte progenitor cells and are restricted to this region in the adult optic nerve. Tenascin is a nonadhesive substrate for oligodendrocytes and their progenitor cells in vitro when offered as a substrate in choice with polyornithine. These observations suggest that tenascin is critical for the establishment and maintenance of the restricted distribution of myelin-forming oligodendrocytes along retinal ganglion cell axons of the mouse.

Tenascin-C inhibits 1 integrin-dependent cell adhesion and neurite outgrowth on fibronectin by a disialoganglioside-mediated signaling mechanism

“…Such molecular mechanism could also be operable in the control of (1) neuronal and glial precursor migration out of the ventricular zone of the neonatal brain (Stallcup et al, 1989;Sheppard et al, 1991;Götz et al, 1997), (2) neuroepithelial cell migration out of the spinal neural tube (Bannerman et al, 1996), (3) corneal cell migration in the developing retina (Kaplony et al, 1988;Sparrow and Barnstable, 1988), or (4) the migration of GD3/β 1 integrin expressing O-2A progenitors (Curtis et al, 1988;Pesheva et al, 1988) in the developing optic nerve (Bartsch et al, 1992b). Disialoganglioside-mediated interference with integrin-dependent adhesion of O-2A cells may also underlie the inhibition of their migration into the retina in the region of lamina cribrosa, demarcating the myelinated from the nonmyelinated part of the optic nerve (Fok-Seang et al, 1995;Kiernan et al, 1996), where TN-C is expressed at this time period (Bartsch et al, 1994). Similar mode of action could be attributed to TN-C in the regulation of axonal growth and plasticity, as disialogangliosides are enriched in the growth cone membrane and synaptosomes (Durrie et al, 1987;Sbaschnig-Agler et al, 1988) and antibody J1/tn2 interferes with the axonal outgrowth of thalamic and cortical neurons (Götz et al, 1997).…”

ALCAM Regulates Mediolateral Retinotopic Mapping in the Superior Colliculus

“…Images were captured on a Leica DM5000B epifluorescence microscope using nonoverlapping ET series filters (Chroma Technology). For in situ hybridization to detect ALCAM or L1 mRNA, sense and antisense probes were generated from psBluescript SK plasmid containing mouse L1 cDNA (Macias et al, 2002) or a 900 bp fragment of mouse ALCAM cDNA (Weiner et al, 2004), and hybridization was performed using digoxigenin-labeled probes as described previously (Bartsch et al, 1994;Garrett and Weiner, 2009).…”

L1 and CHL1 Cooperate in Thalamocortical Axon Targeting

“…Alternatively, cryostat sections from unfixed brains were mounted onto slides and fixed with 4% PFA before being subjected to in situ hybridization analysis. In situ hybridization was performed as described using digoxigenin-labeled probes as described (Bartsch et al 1994).…”