Dendritic and synaptic protection: is it enough to save the retinal ganglion cell body and axon?

J Neuroophthalmol. 2008 Jun;28(2):144-54. doi: 10.1097/WNO.0b013e318177edf0.

Abstract

Glaucoma and other optic neuropathies have been traditionally viewed as diseases of the optic nerve that lead to retinal ganglion cell (RGC) degeneration. Accordingly, the primary aim of neuroprotective strategies has been to preserve RGC axons and soma. RGCs are complex and highly polarized central neurons, and their pathologic response in disease is likely to be an integration of signals from all cellular compartments-axons, soma, dendrites, and synaptic contacts. We focus on the role of dendrites and dendritic spines in normal neuronal function, neurologic disorders, and glaucoma. The need to understand the mechanisms underlying RGC dendrite and synapse degeneration in glaucoma and other optic neuropathies is compelling, as it may provide insight into novel therapeutic strategies to prevent vision loss.

Publication types

  • Review

MeSH terms

  • Animals
  • Axons / metabolism
  • Axons / pathology*
  • Cell Communication / physiology
  • Dendrites / metabolism
  • Dendrites / pathology*
  • Dendritic Spines / metabolism
  • Dendritic Spines / pathology
  • Humans
  • Nerve Degeneration / metabolism
  • Nerve Degeneration / pathology
  • Nerve Degeneration / physiopathology
  • Optic Nerve Diseases / metabolism
  • Optic Nerve Diseases / pathology*
  • Optic Nerve Diseases / physiopathology*
  • Presynaptic Terminals / metabolism
  • Presynaptic Terminals / pathology
  • Retinal Ganglion Cells / metabolism
  • Retinal Ganglion Cells / pathology*
  • Synapses / metabolism
  • Synapses / pathology*