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S.L. Ball, A. Ohtoshi, B.W. Hanzlicek; Evaluation of Inner Retinal Activity in Vsx1–/– Mutant Mice Using c–fos Immunohistochemistry . Invest. Ophthalmol. Vis. Sci. 2006;47(13):155.
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© ARVO (1962-2015); The Authors (2016-present)
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. We have previously shown that monitoring expression of an immediate early gene, c–fos, in amacrine cells can provide useful information regarding inner retinal circuitry when applied to mice with defects in rod photoreceptors and depolarizing bipolar cell pathways. Here we apply this technique to mice with a dysfunctional hyperpolarizing bipolar cell pathway.
Dark adapted mice were exposed to a strobe light stimulus presented at 2 Hz for 60 minutes ranging in intensity from –3.7 to 0.4 log cd sec/m2. Three wild–type (WT) and 3 Vsx1–/– mice were studied. Immediately following light exposure eyes were removed and processed for immunohistochemistry with c–fos anti–serum (Santa Cruz Biotechnology). Using fluorescence microscopy, c–fos–positive cells were viewed and counted in the inner nuclear layer and ganglion cell layer.
In WT mice, the number of inner retinal cells labeled for c–fos increased with increasing stimulus intensity. In Vsx1–/– mice, the number of inner retinal cells labeled for c–fos also increased with increasing stimulus intensity in a fashion comparable to WT mouse retinas. Studies are ongoing to more precisely define the amacrine cell types which express c–fos under these conditions.
We have previously shown that under these experimental conditions c–fos activation is predominantly mediated by rod and cone photoreceptor activation. These results suggest that c–fos activation selectively probes the depolarizing bipolar cell inner retinal circuit as little or no alterations were noted in mice lacking functional hyperpolarizing bipolar cell circuits.
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