Protein synthesis and axonal transport in goldfish retinal ganglion cells during regeneration accelerated by a conditioning lesion Academic Article Article uri icon


MeSH Major

  • Nerve Regeneration
  • Optic Nerve
  • Proteins


  • Axonal outgrowth in goldfish retinal ganglion cells following a testing lesion of the optic axons is accelerated by a prior conditioning lesion. Changes in protein synthesis and axonal transport were examined during the accelerated regeneration. The conditioning lesion was an optic tract cut made 2 weeks prior to the testing lesion, which consisted of a tract cut at the chiasma, so that nerves subjected to either a conditioning lesion ('conditioned nerves') or a sham operation ('sham-conditioned nerves') could be examined in the same animal. In the retinal ganglion cells of conditioned nerves, the incorporation of [3H]proline into protein began to increase between 1 and 8 days after the testing lesion. The amount of fast-transported labeled protein was elevated to about 8 X normal by 1 day after the testing lesion but had decreased to about 3-5X normal at 8 and 22 days. The 8 and 22 day values were not significantly different from those in sham-conditioned nerves or nerves that had received a testing lesion alone. For slow protein transport, the instantaneous amount transported was 15-16 X normal in the conditioned nerves at 1 and 8 days after the testing lesion, and the velocity of slow transport, which was already elevated above normal by 1 day after the testing lesion, was elevated still further by 8 days--to a value in excess of 1.5 mm/day (compared to 0.2-0.4 mm/day in normal animals). We believe that the enhanced outgrowth resulting from the conditioning lesion is due to a transient increase in the amount of fast transport (possibly responsible for a decreased delay in the initiation of sprouting), and a sustained increase in the amount and velocity of slow transport (which may account for an increased rate of elongation).

publication date

  • November 11, 1982



  • Academic Article


Digital Object Identifier (DOI)

  • 10.1016/0006-8993(82)91270-7

PubMed ID

  • 6184129

Additional Document Info

start page

  • 25

end page

  • 37


  • 251


  • 1