RGD Reference Report - Retinal ganglion cells do not extend axons by default: promotion by neurotrophic signaling and electrical activity. - Rat Genome Database

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Retinal ganglion cells do not extend axons by default: promotion by neurotrophic signaling and electrical activity.

Authors: Goldberg, JL  Espinosa, JS  Xu, Y  Davidson, N  Kovacs, GT  Barres, BA 
Citation: Goldberg JL, etal., Neuron 2002 Feb 28;33(5):689-702.
RGD ID: 70671
Pubmed: PMID:11879647   (View Abstract at PubMed)

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.

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
negative regulation of apoptotic process  IDA 70671 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Bcl2  (BCL2, apoptosis regulator)


Additional Information