Abstract
Purpose: :
In mouse models of glaucoma, artificial induction of IOP elevation/lowering may provide key information on susceptibility of retinal ganglion cells to IOP insult. We characterized the dynamics of IOP changes in response to changes of body posture in DBA/2J (D2) and C57BL/6J (B6) mice.
Methods: :
IOP was measured with a Tonolab rebound tonometer in anesthetized (Ketamine/Xylazine) mice of different ages. The magnitude and temporal dynamics of IOP changes for a fixed amount (60 deg) of body tilt was determined in 21 mice/eyes (D2 2 months, n=7, D2 6 months, n=7, D2 10 months n=7, B6 11 months, n=6) by continuously (1-2 minutes intervals) measuring IOP with mice in horizontal position (baseline: 10 min), during 60 deg head-up/head-down body tilting (tilt: 30 min), and again in horizontal position (recovery, 15 min). The magnitude of IOP changes as a function of ± tilt angle (20 deg steps) was determined in 10 D2 mice (4 months: n= 4, 6 eyes; 5.5 months: n=3, 6 eyes, 10 months, n=2, 4 eyes, 12 months, n=1, 2 eyes)
Results: :
Body tilt (60 deg) resulted in an average IOP change of either -5.8 ±0.9 mm Hg (head-up) or +5.4 ±2.3 mm Hg (head-down) independently of age. In B6 mice 11 month old, IOP elevation was 7.5 ± 0.6 mm Hg. IOP change upon tilting had an exponential time-course with a time constant of 3.6 ± 2.2 min (head-down) and 5.5 ± 2.16 min (head-up). IOP lowering-elevation was stable during tilting and returned to baseline conditions upon horizontal repositioning. The magnitude of IOP change in D2 mice was a linear function of the sine of the ± angle of tilt, with a slope of 5.24 ± 0.36 mm Hg/90 deg, and was independent of age.
Conclusions: :
Body tilting in mice induces reproducible/stable IOP changes whose magnitude increases with the angle of tilt. Head-down and head-up tilt induce mirror-symmetric IOP changes, with the exception that the time-course of change is slower for the head-up condition. Body tilt is a promising tool for non-invasive modulation of IOP levels in mouse glaucoma models.
Keywords: stress response • genetics • intraocular pressure