Neuron
Volume 33, Issue 5, 28 February 2002, Pages 689-702
Journal home page for Neuron

Article
Retinal Ganglion Cells Do Not Extend Axons by Default: Promotion by Neurotrophic Signaling and Electrical Activity

https://doi.org/10.1016/S0896-6273(02)00602-5Get rights and content
Under an Elsevier user license
open archive

Abstract

We investigate the signaling mechanisms that induce retinal ganglion cell (RGC) axon elongation by asking whether surviving neurons extend axons by default. We show that bcl-2 overexpression is sufficient to keep purified RGCs alive in the absence of any glial or trophic support. The bcl-2-expressing RGCs do not extend axons or dendrites unless signaled to do so by single peptide trophic factors. Axon growth stimulated by peptide trophic factors is remarkably slow but is profoundly potentiated by physiological levels of electrical activity spontaneously generated within embryonic explants or mimicked on a multielectrode silicon chip. These findings demonstrate that these surviving neurons do not constitutively extend axons and provide insight into the signals that may be necessary to promote CNS regeneration.

Cited by (0)

5

Present address: Millenium Pharmaceuticals, Inc., 75 Sidney Street, Cambridge, Massachusetts 02139.