Abstract
Purpose: :
To characterize the age-related susceptibility to blast-induced optic nerve damage using pattern electroretinography (pERG) in a mouse model of blast wave TBI injury.
Methods: :
Blast injury was produced by exposing anesthetized mice to a 20 psi overpressure wave in a specially constructed blast tank using compressed air to rupture a Mylar membrane. pERG was used to objectively measure retinal ganglion cell function. pERG amplitudes (N35-P50 and P50-N95) and latencies (N35, P50, and N95) were evaluated in control (n=20) and blast-injured mice (n=30) at 1 year of age. Mice were exposed to blast injury at 2 months (n=10), 4 months (n=9) and 7 months (n=11) of age.
Results: :
At 1 year of age, the P50-N95 amplitude in control mice was 8.5±0.5 µV (mean±SEM). At 1 year of age, pERG P50-N95 amplitude was evaluated in all blast treated animals and was significantly decreased compared to the age-matched control mice. P50-N95 amplitude was 6.3±1 µV (p=0.01, t-test; blast at 2 months of age); 5.5±0.6 µV (p=0.001, t-test; blast at 4 months of age), and 6.2±0.6 µV (p=0.008, t-test; blast at 7 months of age). When compared to age-matched controls, the P50-N95 amplitudes of mice injured at 2 months, 4 months, and 7 months of age were reduced by 26.4±11.8%, 35.2±7%, and 27±7.6%, respectively after one year. There was no significant difference in the magnitude of pERG deficits in different age groups after blast exposure (p=0.7; ANOVA).
Conclusions: :
Chronic pERG deficits persist for one year after single blast exposure in a mouse model of blast induced TBI. There was no evidence of increased susceptibility to blast-induced retinal-optic nerve injury associated with age.
Keywords: aging • optic nerve • trauma