Fibrocytes in the cochlear lateral wall and spiral limbus play an important role in transporting K(+) and have the capacity of self-renewal. We showed that acute energy failure in the rat cochlea induced by local administration of the mitochondrial toxin 3-nitropropionic acid (3NP) caused hearing loss in a concentration-dependent manner, mainly due to degeneration of cochlear fibrocytes. We produced long-lasting profound cochlear damage in this model by modifying the 3NP administration protocol and observed morphological changes at 16 weeks after the administration. In the spiral ligament, severe degeneration of fibrocytes was observed in the basal turn, and the levels of the Na,K-ATPase alpha and beta1 subunits and of NKCC1 were decreased in these cells, whereas connexin 26 (Cx26) level increased in the type 1 fibrocytes adjacent to the stria vascularis. In the stria vascularis, levels of Kir4.1 and L-PGDS decreased. In the spiral limbus, severe degeneration of fibrocytes was observed in the middle and basal turns, but NKCC1 and Cx26 were still found in the center of the limbus in the middle turn. These results indicate long-lasting changes in the cochlear lateral wall and spiral limbus, which may compensate for damaged K(+) recycling and protect cells from ATP shortage.
Keywords: 3-Nitropropionic acid; 3-nitropropionic acid; 3NP; ABR; Cochlear fibrocytes; Cx26; Hearing loss; Kir4.1; L-PGDS; Mitochondrial dysfunction; NKCC1; Na-K-Cl cotransporter isoform 1; PBS; Recovery; SSNHL; Stria vascularis; an inwardly rectifying K(+) channel; auditory brainstem response; connexin 26; lipocalin-type prostaglandin D synthase; phosphate buffered saline; sudden sensorineural hearing loss.
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