Incorporation of mouse neural progenitors transplanted into the rat embryonic forebrain is developmentally regulated and dependent on regional and adhesive properties

During development, telencephalic neural progenitors acquire positional specification and give rise to distinct structures such as the striatum and cortex. Here, we examine, in vivo, the influence of developmental stage, cell‐surface molecules and regional differences along the dorso‐ventral and antero‐posterior axes on the selective incorporation of neural progenitors derived from different regions of the developing brain, utilizing a cross‐species in utero transplantation paradigm. Striatal progenitors derived from the embryonic day (E) 12–14 mouse lateral ganglionic eminence (LGE) were observed consistently to incorporate into the developing striatum as early as 24–48 h following intraventricular injection into the E15–17 rat host. By removing cell‐surface molecules from the LGE progenitors, the pattern of incorporation was remarkably different with no preferential striatal incorporation. Cortical progenitors with intact cell‐surface molecules, by contrast, displayed little telencephalic (including striatal) incorporation as compared with precursors from the LGE. However, both progenitors from cortex and LGE incorporated widely into diencephalic and mesencephalic structures. The capacity for integration of precursors derived from the LGE and cortex gradually decreased during development of the host and was minimal in the postnatal day (P) 1 host. Unlike the telencephalic precursors, the vast majority of progenitors derived from the midbrain and cerebellar primordium (with cell‐surface molecules intact) incorporated into diencephalic and midbrain nuclei with only a few cells observed in the telencephalon. These results demonstrate that incorporation of neural progenitors across the ventricular wall in the embryonic host is strictly developmentally regulated, dependent on their position along the antero‐posterior axes and in the case of progenitors from the LGE is mediated by cell‐surface molecules expressed on the transplanted cells.