Inhibition of FGF Receptor Activity in Retinal Ganglion Cell Axons Causes Errors in Target Recognition

Neuron. 1996 Aug;17(2):245-54. doi: 10.1016/s0896-6273(00)80156-7.

Abstract

Native fibroblast growth factor receptor (FGFR) function was inhibited in developing Xenopus retinal ganglion cells (RGCs) by in vivo transfection of a dominant negative FGFR. Axons expressing the dominant negative protein advanced at 60% of the normal speed, but nevertheless navigated appropriately in the embryonic optic pathway. When they neared the optic tectum, however, many axons made erroneous turns, causing them to bypass rather than enter their target. By contrast, RGC axons expressing nonfunctional FGFR mutants entered the tectum correctly. These findings demonstrate a role for FGFR signaling in the extension and targeting of RGC axons and suggest that receptor tyrosine kinase/growth factor interactions play a critical function in establishing initial connectivity in the vertebrate visual system.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Axons / chemistry
  • Axons / physiology*
  • Cell Movement / physiology*
  • Female
  • Microscopy, Video
  • Neurites / physiology
  • Receptors, Fibroblast Growth Factor / antagonists & inhibitors*
  • Receptors, Fibroblast Growth Factor / physiology*
  • Retinal Ganglion Cells / cytology
  • Retinal Ganglion Cells / physiology*
  • Retinal Ganglion Cells / ultrastructure
  • Signal Transduction / physiology*
  • Superior Colliculi / cytology
  • Xenopus laevis

Substances

  • Receptors, Fibroblast Growth Factor