Abstract
Abstract: :
Purpose: Visual information is mediated by multiple pathways in the mouse retina. Mice with functional defects in these pathways provide the opportunity to study their contribution to various aspects of visual function. For example, the nob mouse lacks communication between photoreceptors and depolarizing bipolar cells (DBC) while transducin null mice (Tr-/-) lack rod-mediated function. We have examined how these mutations alter inner retinal activity, by monitoring light-induced expression of an immediate early gene, c-fos, in a subpopulation of amacrine cells. Methods: After overnight dark adaptation, mice were exposed to a strobe light stimulus presented at 2 Hz for 60 min. In different trials, light intensity varied from –2.7 to 0.4 log cd/sec m2. For each stimulus condition, at least 3 wild-type (WT), nob, Tr-/- and Tr+/- mice were studied. Eyes were removed immediately following light exposure and processed for immunohistochemistry with c-fos anti-serum (Santa Cruz Biotechnology). Using light microscopy, c-fos-positive cells were counted in the inner nuclear layer. Results: In all mouse lines, the number of cells labeled for c-fos increased with increasing stimulus intensity. Fewer cells labeled for c-fos in Tr-/- or nob mice than in WT or Tr+/- retinas. In mice exposed to the lowest flash intensities, more cells were labeled in nob than in Tr-/- retinas. At the highest flash intensity more cells were labeled in Tr-/- than in nob retinas. Conclusions: These results indicate that c-fos activation can be used as an assay of inner retinal function and, when applied to mice lacking particular pathways, to elucidate inner retinal circuitry. Our results also indicate that c-fos activation is predominantly mediated by rod DBCs. Differences between Tr-/- and nob mice may reflect the use of an alternative rod pathway spared by the nob defect.
Keywords: retinal connections, networks, circuitry • amacrine cells • animal model