Available only for arXiv papers.
Exposure to intense noise damages both the cochlea and vestibular end organs. Our group previously reported attenuated vestibular short-latency evoked potentials (VsEP) and reduced numbers of calretinin-positive (CR+) calyces in the saccule following noise exposure. Here, we examined rats\' resting head orientation with respect to gravity as well as head stability following a 4-hour exposure to 120 dB SPL noise. We also assessed how behavioral changes are related to changes in VsEP waveforms and calretinin expression in the otoliths to elucidate potential underlying mechanisms. We found significant delays in the VsEP N1 and P2 peak latencies and significant reductions in the N2P3 amplitudes following noise exposure. The number of CR+ calyces in both saccule and utricle were also significantly reduced. The size of the reduction in N2P3 amplitude was significantly correlated to the number of CR+ calyces in the utricle, but not to the saccule. Animals with larger delays in N1 peak latency and/or smaller numbers of CR+ calyces in the utricle following noise showed significant decreases in the average speed of y-axis rotational head motion, while those with smaller changes showed significant increases. In addition, animals with larger noise-induced changes held their heads motionless longer following noise exposure. We hypothesize that noise exposure is inherently destructive to an animal\'s head stability and thereby manifests as an increase in average head speed in mildly to moderately affected animals. But when the damage was large enough, animals exhibited reduced duration and head motion speed as a behavioral adaptation. The noise exposure also significantly altered the pitch angle of head orientation in animals who had the smallest number of CR+ calyces in the saccule, suggesting that saccular irregular afferents, including those that are CR+, are critical in control of head and body posture.