Characterization of retinal regeneration in adult zebrafish following multiple rounds of phototoxic lesion.

Müller glia in the zebrafish retina respond to retinal damage by re-entering the cell cycle, which generates large numbers of retinal progenitors that ultimately replace the lost neurons. In this study we compared the regenerative outcomes of adult zebrafish exposed to one round of phototoxic treatment with adult zebrafish exposed to six consecutive rounds of phototoxic treatment. We observed that Müller glia continued to re-enter the cell cycle to produce clusters of retinal progenitors in zebrafish exposed to multiple rounds of phototoxic light.

Synaptotagmin isoforms confer distinct activation kinetics and dynamics to chromaffin cell granules.

Adrenomedullary chromaffin cells respond to sympathetic nervous system activation by secreting a cocktail of potent neuropeptides and hormones into the circulation. The distinct phases of the chromaffin cell secretory response have been attributed to the progressive fusion of distinct populations of dense core granules with different activation kinetics. However, it has been difficult to define what distinguishes these populations at the molecular level.

Reactive gliosis in the adult zebrafish retina.

In contrast to mammals, zebrafish posses the remarkable ability to regenerate retinal neurons. Damage to the zebrafish retina induces Müller glia to act as stem cells, generating retinal progenitors for regeneration. In contrast, injury in the mammalian retina results in Müller glial reactive gliosis, a characteristic gliotic response that is normally detrimental to vision.