Preservation of cochlear function in Fabp3 (H-Fabp) knockout mice

Abstract

AbstractFatty acid-binding protein 3 (Fabp3) is an intracellular lipid trafficking protein that mediates energy metabolism and long-chain fatty acid-related signaling. Fabp3 is expressed in the spiral ganglion neurons and supporting cells of the organ of Corti. However, it is unclear what role Fabp3 plays in the cochlea. Here, we demonstrated that the ABR thresholds of young and aged Fabp3 knockout mice were unchanged compared with those of wild-type mice. Compared with the wild-type mice, the adult mutant mice demonstrated no differences in their vulnerability to acoustic overexposure. These results suggest that Fabp3 deficiency alone does not adversely affect hearing function