Cholinergic neurones acquire adrenergic neurotransmitters when transplanted into an embryo.

During development, cells become progressively restricted, until they reach their final phenotype. Differentiation was originally thought to be irreversible, but phenotypic plasticity has been observed in a variety of cell types, for example sympathetic neurones, the limb blastema and some glial cell types. A detailed description of the individual steps that lead to expression or reversal of phenotype is essential to understand the molecular events underlying cell differentiation. We examined whether ciliary neurones acquire adrenergic properties when exposed to a permissive embryonic environment. Cholinergic neurones were selectively labelled with a retrogradely transported marker and injected into chick embryos during active neural crest migration. Four to five days after injection, some of the labelled neurones were found in 'adrenergic sites' and had developed catecholamine histofluorescence. The cells had thus accumulated adrenergic neurotransmitters even after differentiation into cholinergic neurones. This result shows that neurotransmitter plasticity occurs in cholinergic neurones and suggests that the neurotransmitter phenotype can be modified by the embryonic environment.

Parasympathetic neurons of salivary gland ganglia in the fetal and postnatal rat are substance P-like immunoreactive.

Substance P-like immunoreactivity (SPLI) of neuron cell bodies is described here in the parasympathetic ganglia of salivary glands in rat fetuses. When grafted to the anterior eye chamber of adult rats, outgrowth of SPLI fibers was also observed around fetal and postnatal ganglia. These observations are significant for the understanding of salivation mechanisms. They also imply the importance of substance P or related compounds in parasympathetic peripheral neurons. The graft experiments indicate a substantial morphological plasticity of these SPLI neurons on perturbation.

Cell division in the ciliary ganglion of quail embryos in situ and after back-transplantation into the neural crest migration pathways of chick embryos.

Embryonic 4- to 15-day-old quail ciliary ganglia (CG) were grafted into the neural crest migration pathway of 2-day-old chick embryos at the adrenomedullary level of the neural axis. This back-transplantation results in dispersion of cells of the implanted ganglion, their migration in the host embryo, and subsequent promotion of their differentiation into a variety of neural-crest-derived cell types including adrenergic cells of the sympathetic ganglia and adrenal medulla. These cells can be recognized in the host through the nuclear marker that they carry. Here, we have analyzed quantitatively the expansion of CG-derived cell population after the graft, and compared cell division in CG after back-transplantation and during normal in situ development over the same period of time. Tritiated-thymidine [( 3H]TdR) incorporation showed that grafted CG cells proliferated during their migration and, to a greater extent, after they had homed to the host structures. Furthermore, proliferative activity of quail cells in the graft was found to be significantly higher than the growth rate of the CG cells in situ during the same period of development. In the quail donor embryo, the birthdate of the CG neurons occurred early in development; from 6 days onward, only nonneuronal cells were still dividing. When back-transplanted, the 4- to 5-day-old CG provided numerous quail cells located in autonomic structures of the host embryo. However, this increase of the total quail cell population and of cell division was reduced when CG were taken from quail donors at progressively later developmental stages. Postmitotic neurons from mature CG were found not to survive under the graft conditions. It is proposed that back-transplantation of the CG stimulates cell division and modifies the developmental programme of still undifferentiated precursor cells which then can give rise to a variety of cell types belonging either to the glial or the autonomic nerve and paraganglionic cell phenotypes, to the exclusion of sensory neurons which never derive from CG grafts.