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M. Nagaraju, V. Porciatti; Head-Up Tilt Reduces IOP and Improves Abnormal PERG in DBA/2J Glaucoma. Invest. Ophthalmol. Vis. Sci. 2008;49(13):1556. doi: https://doi.org/.
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DBA/2J (D2) mice spontaneously develop progressive IOP elevation and retinal ganglion cell (RGC) dysfunction that precedes RGC axon death (Saleh et al, IOVS 2007). We tested the hypothesis that head-up body posture lowers IOP, resulting in improvement of RGC dysfunction.
RGC function was evaluated in anesthetized (Ketamine/Xylazine) D2 mice (2 month old, n= 7, 6 month-old, n= 7, 10 month-old, n= 7) by means of the PERG (IOVS Feb 2007;48(2):745-51). IOP was measured with Tonolab rebound tonometer. IOP and PERG were measured with mice in horizontal position (baseline), during 60 deg head-up body posture (tilted), and again in horizontal position (recovery).
In agreement with previous results (Saleh et al, IOVS 2007), IOP progressively increased and PERG amplitude progressively decreased with increasing age. In all age groups, head-up tilt consistently reduced IOP by ~ 5.5 mm Hg (2 month old: -5.28 ± 0.48 mm Hg; -32.2%; 6 month old: -5.57 ± 0.97 mm Hg, -26.42%; 10 month old: -6.14 ± 0.90 mm Hg, -21.7%) compared to horizontal (P<0.01). Head-up tilt did not induce PERG amplitude changes in 2 month-old mice. By contrast, the abnormal PERG amplitude of 6 month-old mice (-52.7 ± 18.6% compared to the mean amplitude of 2 month old) recovered ~22% (-31.01 ± 31.2% compared to 2 month old, P<0.05); the abnormal PERG amplitude of 10 month-old mice (-74.7 ± 8.8% compared to 2 month old) recovered ~26% (-48.651 ± 10.4% compared to 2 month old, P<0.01). Both IOP and PERG returned to baseline values in the recovery condition. The photopic flash-ERG was similar in all age group and did not change upon tilting.
Recoverable PERG amplitude with IOP lowering in 6 and 10 month old DBA/2J mice implies that age-related loss of RGC function is due to IOP-dependent, reduced responsiveness of viable retinal neurons rather than lack of activity of dead neurons. Head-up tilt represents a non-invasive way to probe the potential for recovery of RGC dysfunction in DBA/2J mice.
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