Fast axonally transported proteins in regenerating goldfish optic nerve: effect of abolishing electrophysiological activity with TTX.

Overview

Blocking neural activity with intraocular tetrodotoxin (TTX) hinders regeneration of goldfish optic axons, and prevents the refinement of the retinotopic map that is formed in the optic tectum. The latter effect is not observed with TTX treatment confined to the first two weeks of regeneration, but is produced when the TTX treatment is delayed until after this time. In the present study, 2-dimensional gel electrophoresis was used to analyse the effects of two different schedules of TTX treatment (0-9 days or 14-32 days) on incorporation of [3H]proline into individual proteins conveyed by fast axonal transport in the optic nerve. The labelling of many of these proteins was somewhat reduced by either schedule of TTX treatment, but a number of proteins showed a larger reduction as a result of the delayed treatment. These included some glycoproteins, as well as a protein of about 45 kDa and pI 4.5, which shows greatly increased synthesis during regeneration, and which is probably identical to the 'growth-associated protein' GAP-43. By contrast, cytoskeletal proteins (alpha- and beta-tubulin and actin) were unaffected by the delayed TTX treatment. It is possible that the differential effects of the early and delayed TTX treatments on various transported proteins may account for differences in the effect of these treatments on the retinotectal projection.