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K.W. Ruether, I. Paradowski, M. Leitges, S. Skosyrski, O. Strauss; Quantitative, but Not Morphological Changes of ERG Rod – and Cone–Responses in PKC–Beta Knock Out Mice . Invest. Ophthalmol. Vis. Sci. 2005;46(13):1194.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: In the rodent retina Ca2+–dependent protein kinase C beta (PKC–beta) has been shown to be localized in different retinal cell layers as cone bipolar cell somata and axons, amacrine and ganglion cells. The present study was performed to elucidate the functional role of PKC–beta in the mouse retina. Methods: 6 PKC–beta knock out mice and 6 controls have been examined by Ganzfeld electroretinograms (ERGs). Scotopic and photopic ERGs were performed in the anaesthetized mice. A–, b, and c–waves were analyzed. The age of the mice was 5 months. Retinal morphology was assessed by light microscopy. Results: Histological examination of the PKC b –/– mouse retina revealed no detectable retinal degeneration. Scotopic b– wave and c–wave amplitudes showed a significant decrease in knock outs compared to controls. In contrast, the cone–response– and a–wave amplitudes were attenuated to a much lesser extent, the difference of the latters not reaching statistical significance. Implicit times and the morphology of the potentials did not show any differences between knock outs and controls Conclusions: Recently we could show that knocking out the mouse PKC–alpha gene leads to a profound change of the scotopic ERG response–characteristics. The shut–off of the rod–b–wave was severely delayed. This effect cannot be observed in PKC–beta knock out mice. However, these animals show a quantitatve effect displaying attenuated ERG amplitudes. Interestingly, this quantative effect was more pronounced in the rod– than in the cone–response. Among other things the attenuation of retinal activity due to knocking out PKC–beta might be relevant as PKC–beta inhibitors are currently investigated as potentially useful drugs to ameliorate diabetic retinopathy.
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