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

Jun Suzuki, Takeshi Ohshima, Naohiro Yoshida, Ryuichi Kimura, Yusuke Takata, Yuji Owada, Toshimitsu Kobayashi, Yukio Katori, Noriko Osumi

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Fatty 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.

Original languageEnglish
Pages (from-to)64-68
Number of pages5
JournalNeuroscience Research
Volume81-82
DOIs
Publication statusPublished - 2014 Apr

Keywords

  • Acoustic overexposure
  • Age-related hearing loss (AHL)
  • Cochlea
  • Fatty acid-binding protein 3 (Fabp3)
  • H-Fabp
  • Noise-induced hearing loss (NIHL)

ASJC Scopus subject areas

  • Neuroscience(all)

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