Elsevier

Developmental Biology

Volume 229, Issue 1, 1 January 2001, Pages 15-30
Developmental Biology

Regular Article
Characterization of CNS Precursor Subtypes and Radial Glia

https://doi.org/10.1006/dbio.2000.9962Get rights and content
Under an Elsevier user license
open archive

Abstract

The role of radial glial cells as guides for migrating neurons is well established, whereas their role as precursor cells is less understood. Here we examined the composition of radial glial cells and their proliferation in the mouse telencephalon during development. We found that almost all radial glial cells proliferate throughout neurogenesis. They consist of three distinct subsets identified by immunostaining for the antigens RC2, the astrocyte-specific glutamate transporter (GLAST), and the brain-lipid-binding protein (BLBP). In addition, RC2, GLAST, and BLBP antisera label precursor cells with different morphologies and thereby cover almost the entire progenitor pool in the developing cerebral cortex. The subsets identified by differential expression of these antigens differ also in their transcription factor expression and cell cycle characteristics. Moreover, the content of BLBP seems correlated to the fate of the progeny. BLBP-negative precursors are detected only during neurogenesis and persist into postnatal stages solely in the rostral migratory stream, a region of ongoing neurogenesis. In contrast, an enriched population of multipotential cells, neurosphere cultures derived from the adult or embryonic telencephalon, is immunoreactive for RC2, GLAST, and BLBP. Taken together, we have identified novel, functionally distinct subsets of CNS precursor cells.

Keywords

cerebral cortex
ganglionic eminence
neurogenesis
gliogenesis
stem cells
brain-lipid-binding protein (BLBP)
astrocyte-specific glutamate transporter (GLAST)
RC2
Mash1
cell cycle

Cited by (0)

1

To whom correspondence should be addressed at Max-Planck-Institute of Neurobiology, Am Klopferspitz 18A, D-82152 Martinsried, Germany. Fax: +49 89 856 1121. E-mail: [email protected].