Fig. 4.

Transient RL-81 IP application 1 week after noise exposure did not alter either wave I amplitude across frequencies or cochlear structure, both assessed 3 weeks post noise exposure. a–f Wave I amplitudes in vehicle vs. RL-81 between sham- and noise-exposed mice for a 10 kHz, b 12 kHz, c 16 kHz, d 20 kHz, e 24 kHz, and f 32 kHz (no significant differences found; see Table 2). g Cochlear whole mount stained with antibodies for MyoVIIa (blue), CtBP2 (red), and GluR2 (green) shows inner hair cells (blue cell bodies with red nucleus), outer hair cells (blue cell bodies only), and ribbon synapses (red presynaptic staining adjacent to green postsynaptic staining). Intact synapses (yellow arrows) are counted when red presynaptic staining is closely opposed by green postsynaptic staining. Orphan ribbons (red arrows) consist of presynaptic puncta that are not opposed by postsynaptic puncta. h, i Representative images of OHCs from the 16 kHz region of vehicle- (h) and RL-81-treated i cochleae. (j), (k) Representative images of the 16 kHz area IHCs with ribbon synapses in vehicle- j and RL-81-treated (k) cochleae. l, m Quantification of IHC l and OHC m survival from vehicle- and RL-81-treated mice. n, o Quantification of intact ribbon n and orphan ribbon synapses o per IHC of vehicle- and RL-81-treated mice. Vehicle N = 5, RL-81 N = 4; 2-way ANOVA (no significant differences were found)