Serotonin inhibits outgrowth of goldfish retina and impairs the trophic effect of taurine.

The regeneration of explants prepared from goldfish retinas with a prior crush of the optic nerve is stimulated by the sulphur amino acid, taurine. Serotonin has been reported to modify survival, proliferation, and outgrowth of nervous tissue. In the present work we evaluated the effect of serotonin and some serotonergic agonists on the neuritic outgrowth from goldfish retinal explants. Serotonin, its precursor, 5-hydroxytryptophan, and the 5HT1A receptor agonists, 8-hydroxy-2-(di-n-propylamino)tetralin and buspirone, inhibited the outgrowth. The blockers of serotonin uptake, imipramine and citalopram, were also inhibitors of neurite sprouting. Imipramine favoured the inhibitory effect of serotonin at 10 days in culture. The concentration of serotonin and its metabolite, 5-hydroxyindoleacetic acid, decreased in the retina at 3 and 5 days after the crush of the optic nerve. Serotonin levels started to recover after 5 days post-lesion, and the metabolite also increased. This indicates that the lesion increases the turnover rate of serotonin and this may be related to its role in regeneration. Serotonin concentration was elevated by the intraocular administration of its precursor, 5-hydroxytryptophan, indicating that the capacity for synthesis was preserved after the crush, but that it was smaller in the post-lesioned retinas. The trophic effect of taurine was impaired by a low concentration of serotonin, probably by opposing the final effect on growth via different targets. These results support a role of serotonin in the regeneration of goldfish retina probably through 5HT1A receptors.