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NF-kappa B activation following optic nerve transection

J S Choi1, K Y Sungjoo, C K Joo

  • 1Department of Ophthalmology, College of Medicine, Catholic University, Seoul, Korea.

Korean Journal of Ophthalmology : KJO
|October 1, 1998
PubMed
Summary

Optic nerve transection in rats induces retinal ganglion cell (RGC) death via apoptosis. This neuronal cell death involves time-dependent activation of nuclear factor-kappa B (NF-kappa B).

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Area of Science:

  • Neuroscience
  • Ophthalmology
  • Cell Biology

Background:

  • Retinal ganglion cells (RGCs) are crucial for visual processing.
  • Neuronal cell death, particularly apoptosis, is implicated in retinal diseases.
  • The role of nuclear factor-kappa B (NF-kappa B) in RGC survival and death requires further elucidation.

Purpose of the Study:

  • To investigate in vivo neuronal cell death in the retina after optic nerve injury.
  • To determine the involvement of NF-kappa B activation in retinal ganglion cell degeneration.

Main Methods:

  • Adult rats underwent optic nerve transection 5 mm from the eyeball.
  • Retinal ganglion cell morphology was analyzed using light and electron microscopy.
  • NF-kappa B activation (p50 and p65 subunits) was assessed via immunohistochemistry at 7 and 14 days post-axotomy.

Main Results:

  • Optic nerve axotomy led to the degeneration of retinal ganglion cells.
  • Dying cells exhibited pyknotic nuclei, indicative of apoptosis.
  • Prominent, time-dependent activation of NF-kappa B was observed in the retina post-axotomy.

Conclusions:

  • Retinal ganglion cell death following optic nerve injury involves apoptosis.
  • Axotomy-induced NF-kappa B activation is a key event in this process.
  • NF-kappa B activation may mediate the apoptosis of retinal ganglion cells.

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