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T.-H. Chou, M. Nagaraju, V. Porciatti; The PERG Phenotype of DBA/2J Mice Compared to C57BL/6J Mice. Invest. Ophthalmol. Vis. Sci. 2008;49(13):719. doi: https://doi.org/.
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© ARVO (1962-2015); The Authors (2016-present)
DBA/2J (D2) mice spontaneously develop an iris disease resulting in progressive IOP elevation and retinal ganglion cell (RGC) loss. C57BL/6J (B6) mice carrying D2-derived Gpnmb and Tyrp 1 genes develop iris disease and IOP elevation similar to D2 that does not result in RGC loss, suggesting that genetic context determines susceptibility to IOP elevation (Anderson et al, BMC biology, 2006). We characterized baseline differences in RGC function between pre-glaucomatous (2-4 month old) D2 mice and B6 mice by comparing the spatial-temporal characteristics of the PERG.
The PERG was recorded from both eyes of anesthetized (Ketamine/Xylazine) mice (D2, n=10; B6, n= 10) as a function of spatial frequency, temporal frequency, and contrast (IOVS 2007,48:745-51). IOP was measured with a Tonolab tonometer.
In both D2 and B6 mice, the PERG amplitude progressively decreased with increasing spatial frequency, increasing temporal frequency and decreasing contrast, to reach the noise level at values that were considered as corresponding measures of acuity, contrast threshold, and temporal resolution. D2 and B6 mice had similar acuity in c/deg (D2= 0.57, 95% C.I.= 0.4-1.0; B6= 0.59, 95% C.I.= 0.4-1.0), contrast threshold (D2= 0.2, 95%C.I.= 0.15-0.25; B6= 0.15, 95% C.I.= 0.09-0.18) and temporal resolution in Hz (D2= 11.5, 95% C.I.= 8.3-17.7; B6= 8.9, 95% C.I.= 6.7-15.8). However, the contrast transfer function of PERG amplitude and latency radically differed between D2 and B6, suggesting relatively poorer contrast gain control in D2 mice. In addition, D2 mice had considerably longer PERG latency (D2=116.2 ± 7.2 ms, B6=91.8 ±9.5 ms, P<0.001) but similar Flash-ERG latency, compared to B6.
Pre-glaucomatous D2 mice and B6 mice have similar IOP and similar number of RGCs, as well as similar Flash ERG amplitude, PERG amplitude and PERG spatial-temporal thresholds. However, reduced PERG contrast gain and longer PERG latency of D2 mice, compared to B6, indicate baseline differences in RGC function that may have a counterpart in different susceptibility to IOP elevation. Caution is needed when using B6 mice as non-glaucomatous control for D2 mice.
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