17 research outputs found

    GAP, PPI, and startle only ratios from a representative tinnitus<sup>(+)</sup>, tinnitus<sup>(</sup><sup>−)</sup> and control rat.

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    <p>Gap-detection data showed tinnitus at 6–8 and 26–28 kHz in the tinnitus<sup>(+)</sup> rat (A), which was unaccompanied by same-frequency impairment in PPI (B), although PPI showed auditory detection impairment at 14–16 kHz. Neither the tinnitus<sup>(−)</sup> (C–D) nor the control rat (E–F) demonstrated tinnitus or auditory detection deficits. Error bars represent the standard error of the mean (SEM). * indicates p<0.05 between pre- and post-GAP, and p>0.05 between post-GAP and post-Stl-Only.</p

    Startle force for the tinnitus<sup>(+)</sup>, tinnitus<sup>(</sup><sup>−)</sup> and control groups.

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    <p>The tinnitus<sup>(+)</sup> group only demonstrated enhanced startle force during BBN background noise at 1 to 2 weeks post-exposure, but showed a dramatic increase during all carrier bands at 5 to 6 weeks (A). Enhanced startle force without background noise was also seen to a small extent at 1 to 2 weeks post-exposure, but to a much greater extent at 5 to 6 weeks (B). The tinnitus<sup>(−)</sup> group demonstrated no startle force changes (C–D) except for a decrease at 1 to 2 weeks near 26–28 kHz PPI (C–D). The control group showed no startle force changes (E–F) except for an increase at 5–6 weeks during BBN noise (E–F). The tinnitus<sup>(+)</sup> group by far showed the greatest change in startle force, suggesting hyperacusis-like behavior. All groups showed a sensitization to startle force during background noise, as evidenced by stronger startle force during gap-detection testing (background noise present) compared to PPI testing (background noise absent). For PPI tests, all startle only conditions were identical and were organized by the closest frequency of prepulse incidence to maintain similar comparison to gap-detection. Error bars represent SEM. * indicates p<0.05.</p

    Morris water maze escape latency and probe trial data.

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    <p>No significant differences were seen between the tinnitus<sup>(+)</sup>, tinnitus<sup>(−)</sup> and control groups in escape latency (A), probe trial target zone entries (B), probe trial target zone time (C), and velocity (D). This indicated similar spatial learning and memory across groups. Error bars represent SEM.</p

    Correlation between ABR thresholds and GAP ratios for tinnitus<sup>(+)</sup> (A), tinnitus<sup>(−)</sup> (B), and control (C) groups.

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    <p>No groups exhibited a significant correlation, suggesting that although tinnitus<sup>(+)</sup> rats had more overall hearing loss (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0075011#pone-0075011-g004" target="_blank">Figure 4</a>), it was not the only factor accounting for elevated GAP ratios and thus behavioral manifestation of tinnitus.</p

    Auditory brainstem responses from the exposed left ear (A) and unexposed right ear (B).

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    <p>In the exposed ear (A), both the tinnitus<sup>(+)</sup> and tinnitus<sup>(−)</sup> groups showed significant threshold shifts across tone-burst frequencies at 1 and 8 weeks post-exposure, with the strongest elevations occurring at 12 and 16 kHz. Overall, the tinnitus<sup>(+)</sup> group had significantly higher hearing thresholds than the tinnitus<sup>(−)</sup> group, although the thresholds were not significantly higher at any individual frequency or click. (B) No significant threshold shifts were seen in the unexposed ear for tinnitus<sup>(+)</sup> and tinnitus<sup>(−)</sup> groups. The control group showed no changes in either ear (A–B). Error bars represent SEM.</p

    Time course of blast-induced injury in the rat auditory cortex

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    <div><p>Blast exposure is an increasingly significant health hazard and can have a range of debilitating effects, including auditory dysfunction and traumatic brain injury. To assist in the development of effective treatments, a greater understanding of the mechanisms of blast-induced auditory damage and dysfunction, especially in the central nervous system, is critical. To elucidate this area, we subjected rats to a unilateral blast exposure at 22 psi, measured their auditory brainstem responses (ABRs), and histologically processed their brains at 1 day, 1 month, and 3-month survival time points. The left and right auditory cortices was assessed for astrocytic reactivity and axonal degenerative changes using glial fibrillary acidic protein immunoreactivity and a silver impregnation technique, respectively. Although only unilateral hearing loss was induced, astrocytosis was bilaterally elevated at 1 month post-blast exposure compared to shams, and showed a positive trend of elevation at 3 months post-blast. Axonal degeneration, on the other hand, appeared to be more robust at 1 day and 3 months post-blast. Interestingly, while ABR threshold shifts recovered by the 1 and 3-month time-points, a positive correlation was observed between rats’ astrocyte counts at 1 month post-blast and their threshold shifts at 1 day post-blast. Taken together, our findings suggest that central auditory damage may have occurred due to biomechanical forces from the blast shockwave, and that different indicators/types of damage may manifest over different timelines.</p></div

    Correlation between post-blast day 1 ABR thresholds and averaged bilateral astrocyte counts of the 1-month group.

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    <p>A significant positive correlation was observed between ABR thresholds and astrocyte counts (p = 0.04), suggesting a putative relationship between initial hearing loss and later-manifesting central auditory damage.</p

    Auditory brainstem response thresholds in blast- and sham-exposed rats show temporary, blast-induced threshold elevations.

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    <p>For the 1 day post-blast group (1 D PB), significant threshold shifts were observed across clicks and all tone-burst frequencies in the blast-exposed ear (left ear). For the 1- and 3-month post-blast groups (1 Mo PB and 3 Mo PB), however, thresholds were similar to those of sham-exposed rats. There were no significant threshold shifts in the protected ear (right ear) following blast exposure at any time point. Error bars represent standard error of the mean.</p

    ABR hearing thresholds for tinnitus<sup>(+)</sup>, tinnitus<sup>(-)</sup>, and control rats prior to intense noise or sham exposure, and on post-exposure day 0 and post-exposure week 7.

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    <p>Thresholds were elevated across all frequencies in tinnitus<sup>(+)</sup> and tinnitus<sup>(-)</sup> rats at post-exposure day 0, revealing immediate and significant hearing loss. By post-exposure week 7, however, thresholds recovered to pre-exposure levels. At all time points, thresholds were similar between tinnitus<sup>(+)</sup> and tinnitus<sup>(-)</sup> rats. There were no threshold elevations in control rats. Error bars represent standard error of the mean.</p

    Licking rates over time for tinnitus<sup>(+)</sup>, tinnitus<sup>(-)</sup>, and control rats during narrowband sound trials (A-E).

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    <p>Tinnitus<sup><b>(+)</b></sup> refers to rats that later exceeded 1 lick/trial for one or more silent trial categories over weeks 5 through 7 weeks following noise exposure; tinnitus<sup><b>(-)</b></sup> refers to noise-exposed rats that did not meet that criteria. No significant changes in sound trial licking were observed for any group of rats.</p
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