The prosencephalon, or embryonic forebrain, grows within a mesenchymal matr
ix of local paraxial mesoderm and of neural crest cells (NCC) derived from
the posterior diencephalon and mesencephalon. Part of this NCC population f
orms the outer wall of capillaries within the prosencephalic leptomeninges
and neuroepithelium itself. The surgical removal of NCC from the anterior h
ead of chick embryos leads to massive cell death within the forebrain neuro
epithelium during an interval that precedes its vascularization by at least
36 hours. During this critical period, a mesenchymal layer made up of inte
rmingled mesodermal cells and NCC surround the neuroepithelium. This layer
is not formed after anterior cephalic NCC ablation, The neuroepithelium the
n undergoes massive apoptosis. Cyclopia ensues after forebrain deterioratio
n and absence of intervening frontonasal bud derivatives. The deleterious e
ffect of ablation of the anterior NC cannot be interpreted as a deficit in
vascularization because it takes place well before the time when blood vess
els start to invade the neuroepithelium. Thus the mesenchymal layer itself
exerts a trophic effect on the prosencephalic neuroepithelium, In an assay
to rescue the operated phenotype, we found that the rhombencephalic but not
the truncal NC can successfully replace the diencephalic and mesencephalic
NC. Moreover, any region of the paraxial cephalic mesoderm can replace NCC
in their dual function: in their early trophic effect and in providing per
icytes to the forebrain meningeal blood vessels, The assumption of these ro
les by the cephalic neural crest may have been instrumental in the rostral
expansion of the vertebrate forebrain over the course of evolution.