Welcome to the new version of CaltechAUTHORS. Login is currently restricted to library staff. If you notice any issues, please email coda@library.caltech.edu
Published July 17, 1992 | public
Journal Article

Membrane depolarization induces p140^(trk) and NGF responsiveness, but not p75^(LNGFR), in MAH cells

Abstract

Nerve growth factor (NGF) is required for the maturation and survival of sympathetic neurons, but the mechanisms controlling expression of the NGF receptor in developing neuroblasts have not been defined. MAH cells, an immortalized sympathoadrenal progenitor cell line, did not respond to NGF and expressed neither low-affinity NGF receptor (p75) nor p140trk messenger RNAs. Depolarizing concentrations of potassium chloride, but none of a variety of growth factors, induced expression of p140trk but not p75 messenger RNA. A functional response to NGF was acquired by MAH cells under these conditions, suggesting that expression of p75 is not essential for this response. Depolarization also permitted a relatively high proportion of MAH cells to develop and survive as neurons in fibroblast growth factor and NGF. These data establish a relation between electrical activity and neurotrophic factor responsiveness in developing neurons, which may operate in the functioning of the mature nervous system as well.

Additional Information

© 1992 American Association for the Advancement of Science. 6 April 1992; Accepted 5 June 1992. We thank L. Parada for the Trk cDNA probe, E. M. Johnson for monoclonal antibody 192-1g, M. Chao for the p75 probe, and G. Yancopoulos (Regeneron) for BDNF and NT-3; R. Diamond for performing flow cytometric analysis; S. Padilla and M. Sylber for technical assistance; D. Stemple for helpful comments and suggestions; and K. Zinn and P. Patterson for comments on the manuscript. This work was supported by NIH grant NS23476. S.J.B. was supported by funds from the PEW Neurosciences program. D.J.A. is an assistant investigator and J.V. is an associate of the Howard Hughes Medical Institute.

Additional details

Created:
August 20, 2023
Modified:
October 19, 2023