Sympathetic ganglia are primarily composed of noradrenergic neurons and satellite glial cells. Although both cell types originate from neural crest cells, the identities of the progenitor populations at intermediate stages of the differentiation process remain to be established. Here we report the identification in vivo of glial and neuronal progenitor cells in postnatal sympathetic ganglia, using mouse superior cervical ganglia as a model system. There are significant levels of cellular proliferation in mouse superior cervical ganglia during the first 18 days after birth. A majority of the proliferating cells express both nestin and brain lipid-binding protein (BLBP). BrdU fate-tracing experiments demonstrate that these nestin and BLBP double positive cells represent a population of glial progenitors for sympathetic satellite cells. The glial differentiation process is characterized by a marked downregulation of nestin and upregulation of S100, with no significant changes in the levels of BLBP expression. We also identify a small number of proliferating cells that express nestin and tyrosine hydroxylase, a key enzyme of catecholamine biosynthesis that defines sympathetic noradrenergic neurons. Together, these results establish nestin as a common marker for sympathetic neuronal and glial progenitor cells and delineate the cellular basis for the generation and maturation of sympathetic satellite cells. Keywords noradrenergic neurons; satellite cells; superior cervical ganglia; postnatal sympathetic developmentThe sympathetic nervous system is composed of sympathetic ganglia and the adrenal medulla, a specialized sympathetic ganglion containing secretory chromaffin cells. Sympathetic ganglia of mammals are organized into two paravertebral chains that span from cervical to sacral regions, with the ganglia being interconnected with pre-and postganglionic sympathetic nerve fibers. Sympathetic ganglia contain two major cell types, neurons and glial cells. Most mammalian sympathetic neurons use noradrenaline as a neurotransmitter and, thus, are called noradrenergic neurons. These neurons are commonly marked by their expression of tyrosine hydroxylase (TH) that catalyzes the rate-limiting step (Cocchia and Michetti, 1981).It is well established that sympathetic neurons and glia are derived from neural crest cells (Anderson, 1989;LaBonne and Bronner-Fraser, 1998;Le Douarin and Dupin, 1993), a transient, highly migratory population of multipotent stem/progenitor cells. The neural crest can be divided into four regions along the anterior-posterior axis: cranial, vagal, trunk, and lumbosacral neural crest. During sympathetic development, neural crest cells, mainly from the trunk region of the neural crest, migrate ventrally and aggregate adjacent to the dorsal aorta to form the primary sympathetic chain. A subpopulation of the cells then undergo dorsal migration to form the paravertebral sympathetic ganglia where they differentiate into sympathetic neurons and glial cells (Francis and Landis, 1999;Kirby and Gilmore...

We used fluorescence in situ hybridization (FISH) to study the positions of human chromosomes on the mitotic rings of cultured human lymphocytes, MRC-5 fibroblasts, and CCD-34Lu fibroblasts. The homologous chromosomes of all three cell types had relatively random positions with respect to each other on the mitotic rings of prometaphase rosettes and anaphase cells. Also, the positions of the X and Y chromosomes, colocalized with the somatic homologues in male cells, were highly variable from one mitotic ring to another. Although random chromosomal positions were found in different pairs of CCD-34Lu and MRC-5 late-anaphases, the separations between the same homologous chromosomes in paired late-anaphase and telophase chromosomal masses were highly correlated. Thus, although some loose spatial associations of chromosomes secondary to interphase positioning may exist on the mitotic rings of some cells, a fixed order of human chromosomes and/or a rigorous separation of homologous chromosomes on the mitotic ring are not necessary for normal mitosis. Furthermore, the relative chromosomal positions on each individual metaphase plate are most likely carried through anaphase into telophase.

Abstract-We performed an initial screen of 11 rat strains by use of a standard balloon injury to the left iliac artery to observe whether genetically determined differences existed in the development of neointimal hyperplasia. Neointimal hyperplasia was assayed 8 weeks after the vascular injury on coded microscopic sections. Statistically significant differences in the percentages of the vascular wall cross-sectional areas composed of intima (percentage intima) secondary to neointimal hyperplasia were noted among the different rat strains (PϽ0.02), with the Brown-Norway (BN), Dark Agouti, and Milan normotensive strain rats having the highest and the spontaneously hypertensive rats (SHR) having the lowest percentages of intima. In a separate experiment, F 1 hybrids of SHRϫBN strains and parental BN and SHR underwent the vascular injury, and the parental strains again showed a statistically significant difference from one another in the mean percentage of intima (PϽ0.0001). The F 1 hybrids showed an average percentage of intima intermediate between those of the parental strains. The average lumen size of the injured BN vessels were significantly smaller than that of the noninjured control vessels (Pϭ0.044), but this significance disappeared when the circular areas of these vessels were calculated without taking neointimal growth into consideration (Pϭ0.649). These results provide the groundwork for a genetic linkage analysis to identify the genes that influence the development of neointimal hyperplasia after vascular injury. (Circ Res. 1999;84:1252-1257.)