Fig. 7.

Traumatic noise exposure activates CaMKI in OHCs of the basal turn of CBA/J mice. A OHCs of the basal region display immunolabeling for p-CaMKI (T177, red) in the cuticular plate of structurally damaged OHCs when processed 1–3 h after completion of traumatic noise exposure compared to control mice without the exposure. The representative images show the hook and lower basal turn and are representative of 6 mice each. PTSN: permanent threshold shift noise exposure; scale bar = 10 µm. A’ the enlarged four OHCs show immunolabeling for p-CaMKI (Th177) in structurally damaged OHCs (2, 3), but not in intact OHCs (1) or scars of lost OHCs (4). B Counts of the number of OHCs displaying p-CaMKI (Thr177) immunolabeling in the hook and lower basal turns of the cochlear duct confirms a significant increase 1–3 h after completion of PTSN. Data are presented as means + SD. The number of animals in each group is indicated in the bar graph. ***p < 0.001. C Western blots using whole cochlear tissue homogenates reveal specificity for CaMKKβ and p-CaMKI (T177) but show no change in band densities for p-CaMKI (T177) examined 1–3 h after the noise exposure compared with unexposed controls. GAPDH serves as the loading control. The molecular weights are indicated to the right of the bands. Data are presented as means + SD. The number of animals in each group is indicated in the bar graphs, ns: not significant