Glaucomatous optic neuropathy: when glia misbehave

Neuroscientist. 2003 Dec;9(6):485-95. doi: 10.1177/1073858403253460.


The loss of vision in the human eye disease, glaucoma, is due to degeneration of the axons of the retinal ganglion cells. In glaucoma, reactive astrocytes in the optic nerve head contain inducible nitric oxide synthase, which apparently produces excessive nitric oxide that damages the axons. The astrocytes respond to the elevated intraocular pressure that is characteristic of the disease. An important signal transduction pathway for the induction of nitric oxide synthase in response to pressure is the epidermal growth factor receptor tyrosine kinase. Pharmacological inhibition of the activity or the induction of inducible nitric oxide synthase may provide neuroprotection for the treatment of glaucoma.

Publication types

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

MeSH terms

  • Animals
  • ErbB Receptors / metabolism
  • Glaucoma / etiology
  • Glaucoma / pathology*
  • Humans
  • Intraocular Pressure
  • Neuroglia / pathology*
  • Nitric Oxide / metabolism
  • Nitric Oxide Synthase / metabolism
  • Nitric Oxide Synthase Type II
  • Optic Nerve Diseases / complications
  • Optic Nerve Diseases / pathology*
  • Retinal Ganglion Cells / pathology
  • Signal Transduction / physiology*


  • Nitric Oxide
  • NOS2 protein, human
  • Nitric Oxide Synthase
  • Nitric Oxide Synthase Type II
  • ErbB Receptors