Send to

Choose Destination
See comment in PubMed Commons below
Dev Biol. 1996 Apr 10;175(1):184-90.

Environmental signals influence expression of a cortical areal phenotype in vitro independent of effects on progenitor cell proliferation.

Author information

  • 1Department of Anatomy and Neurobiology, Medical College of Pennsylvania, Philadelphia 19129, USA.


We have shown previously that, in vitro, cortical progenitor cells isolated from specific locations of the cerebral wall can adopt area-specific fates, assayed by expression of the limbic system-associated membrane protein (LAMP; R. T. Ferri and P. Levitt, Cereb. Cortex 3, 187-198, 1993). Progenitors destined to produce LAMP neurons, however, will differentiate to express the limbic molecular phenotype if grown with TGFalpha and collagen type IV (R. T. Ferri and P. Levitt, Development 121, 1151-1160, 1995), while other signals fail to induce LAMP. The present study used BrdU labeling of progenitor cells to examine whether modulation of LAMP expression was paralleled by predictable changes in cell proliferation. The general pattern of proliferation is similar under a variety of culture conditions: approximately half the cells are mitotic, and activity is always highest during the first 24 hr in vitro, with little cell division occurring by the third day. Moreover, the rate of proliferation, in the presence or absence of TGFalpha, is the same on all substrates tested, with the exception of laminin. The TGFalpha/collagen type IV signaling system that induces LAMP expression by the precursors has no modulating effect on their proliferative kinetics. Nonetheless, only progenitors that are mitotically active respond to LAMP-inducing signals; only 60% of the neurons, representing those that have divided at least once in culture, can be induced to express LAMP. The data suggest that while specific signals affect choice of area phenotype during the cell cycle, they do so in the absence of major changes in proliferative behavior.

[PubMed - indexed for MEDLINE]
Free full text
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center