Progression of Vestibular Deficits Following Moderate-Intensity Blast Overpressure in Rats
摘要
Military personnel and veterans exposed to blast overpressure waves frequently report vestibular symptoms, including dizziness, vertigo, and imbalance. Although blast exposure is known to disrupt vestibular function, how vestibular deficits develop over time, particularly at the level of vestibular afferent signaling, remains unclear.
MethodsIn this study, we used an ear-blast model to investigate the early injury responses and progression of vestibular deficits following a single, moderate-intensity blast exposure (20 PSI) in male and female Long-Evans rats. Vestibular function was assessed using single-unit recordings from vestibular afferents and vestibulo-ocular reflex (VOR) testing.
ResultsBlast exposure produced progressive changes in vestibular afferent activity in both male and female rats. In males, spontaneous firing rates remained unchanged, whereas females showed a reduction at 1 day and 14 days post-blast. In both sexes, firing irregularity increased, and a greater proportion of afferents became less responsive to head rotation and translation. Although gains and phases of the remaining canal and otolith afferents were preserved, response distortion increased following blast exposure, indicating reduced precision of vestibular afferents’ encoding of head movement. Despite the impairments in vestibular nerve activity, steady-state rotational and translational VOR gains remained largely unchanged, with only moderate phase changes up to 56 days post-blast. However, a subset of animals exhibited reduced step rotational VOR gains and earlier quick phase responses following blast exposure. Morphological analysis revealed stereocilia damage, significant loss of saccular hair cells, and astrocytic activation in the central vestibular nuclei.
ConclusionTogether, these findings indicate that blast-induced vestibular injury involves both peripheral and central components, with progressive changes in vestibular afferent activity that could influence sensory inputs to the CNS.