The retinas of adult teleost fish can regenerate neurons
following a chemical or mechanical injury. Previous studies
have demonstrated that mechanical excision of fish retina
induces a hyperplasia within the retinal sheet, including
the formation of a proliferative blastema from whence new
retinal cells are produced to fill the excision site. The
current study was designed to address two issues regarding
injury-induced retinal hyperplasia: (1) Retinas of adult
zebrafish can regenerate following a surgical excision,
but compared to other fish they contain very few proliferative
cells: Might retinal injury in adult zebrafish therefore
induce minimal, or perhaps no, hyperplasia? (2) The fate
of injury-induced, proliferative retinal cells outside
surgical excision sites has yet to be determined. Do such
cells produce retinal neurons? Evidence is presented that
mechanical injury to the adult zebrafish retina induces
a dramatic increase in the number of proliferative cells
both within and external to the lesion site, and some of
these cells apparently migrate within the radial dimension
of the retina. Evidence is also presented that injury-induced
proliferative cells outside a lesion site can produce retinal
neurons—including cone photoreceptors, interplexiform
cells, and amacrine cells—that are incorporated into
the extant retina. The results suggest that the adult zebrafish
retina contains a latent population of cells that is induced
to proliferate following retinal injury, and that these cells
might represent a novel avenue for pluripotent neurogenesis
within the intact adult teleost retina.