Cell adhesion mechanisms in gangliogenesis studied in avian embryo and in a model system.

Neural crest cells undergo rapid changes in their cell-to-cell and cell-to-extracellular matrix adhesion during the ontogeny of the peripheral nervous system. The mechanisms of adhesion have been analyzed to assess the respective roles played by the cell adhesion molecules (CAMs) and the differentiated junctions. Crest cells which lose their terminal bar junctions after emigration from the neural tube contain only very few gap junctions during gangliogenesis. The calcium-dependent cell adhesion molecules, L-CAM, disappear from the neural crest and never reappear in crest cell derivatives. In contrast, the number of calcium-independent cell adhesion molecules, N-CAM, diminishes transiently during the migratory phase. In vitro, N-CAM is expressed de novo either just before or at the onset of aggregation into autonomic ganglion rudiments, whereas it is delayed in the dorsal root ganglion cells. In vitro, N-CAM mediates the calcium-independent aggregation mechanism; the rate of aggregation is, however, similar whether crest cells are derived from well-spread cultures or from two- and three-dimensional clusters. Crest cells also exhibit a calcium-dependent mechanism of adhesion controlled by molecules differing from N-CAM but which may codistribute on many different cell types during embryogenesis. These two classes of cell adhesion molecules are present on the surface of neural precursors prior to their differentiation into neurons and glial cells.