Display options
Share it on

Clin Exp Otorhinolaryngol. 2012 Sep;5(3):117-21. doi: 10.3342/ceo.2012.5.3.117. Epub 2012 Aug 27.

Decreased Immunoreactivities of the Chloride Transporters, KCC2 and NKCC1, in the Lateral Superior Olive Neurons of Kanamycin-treated Rats.

Clinical and experimental otorhinolaryngology

Myung-Whan Suh, Seung Cheol Ahn

Affiliations

  1. Department of Otorhinolaryngology-Head & Neck Surgery, Dankook University College of Medicine, Cheonan, Korea.

PMID: 22977707 PMCID: PMC3437411 DOI: 10.3342/ceo.2012.5.3.117

Abstract

OBJECTIVES: From our previous study about the weak expressions of potassium-chloride (KCC2) and sodium-potassium-2 chloride (NKCC1) co-transporters in the lateral superior olive (LSO) in circling mice, we hypothesized that partially damaged cochlea of circling mice might be a cause of the weak expressions of KCC2 or NKCC1. To test this possibility, we reproduced the altered expressions of KCC2 and NKCC1 in the LSO of rats, whose cochleae were partially destroyed with kanamycin.

METHODS: Rat pups were treated with kanamycin from postnatal (P)3 to P8 (700 mg/kg, subcutaneous injection, twice a day) and sacrificed for immunohistochemical analysis, scanning electron microscope (SEM) and auditory brain stem response.

RESULTS: The SEM study revealed partially missing hair cells in P9 rats treated with kanamycin, and the hearing threshold was elevated to 63.8±2.5 dB SPL (4 ears) at P16. Both KCC2 and NKCC1 immunoreactivities were more prominent in control rats on P16. On 9 paired slices, the mean densities of NKCC1 immunoreactivities were 118.0±1.0 (control) and 112.2±1.2 (kanamycin treated), whereas those of KCC2 were 115.7±1.5 (control) and 112.0±0.8 (kanamycin treated).

CONCLUSION: We concluded that weak expressions of KCC2 and NKCC1 in circling mice were due to partial destruction of cochleae.

Keywords: Cochlea; KCC2; Kanamycin; Lateral superior olive; NKCC1

References

  1. J Neurobiol. 1997 Nov 20;33(6):781-95 - PubMed
  2. Comp Med. 2001 Dec;51(6):550-4 - PubMed
  3. J Neurosci. 2003 Aug 20;23(20):7516-24 - PubMed
  4. J Physiol. 1996 Jul 15;494 ( Pt 2):451-64 - PubMed
  5. Teratology. 1984 Feb;29(1):57-71 - PubMed
  6. Arch Otorhinolaryngol. 1980;226(3):129-33 - PubMed
  7. Acta Otolaryngol. 2007 Mar;127(3):244-51 - PubMed
  8. Nature. 1999 Jan 21;397(6716):251-5 - PubMed
  9. Clin Exp Otorhinolaryngol. 2011 Mar;4(1):18-23 - PubMed
  10. J Neurophysiol. 1991 Feb;65(2):247-63 - PubMed
  11. Int J Dev Neurosci. 1990;8(4):481-90 - PubMed
  12. Neurosci Res. 2008 Dec;62(4):270-7 - PubMed
  13. Exp Anim. 2002 Apr;51(2):167-71 - PubMed
  14. J Neurosci. 2008 Nov 26;28(48):13003-7 - PubMed
  15. J Neurosci. 2003 May 15;23(10):4134-45 - PubMed
  16. Acta Otolaryngol. 1979;88(5-6):359-68 - PubMed
  17. J Neurosci. 1992 Oct;12(10):3935-45 - PubMed
  18. Hear Res. 1980 Mar;2(2):111-3 - PubMed
  19. J Neurophysiol. 1998 Nov;80(5):2608-20 - PubMed
  20. Biochem Biophys Res Commun. 2011 Feb 11;405(2):162-7 - PubMed
  21. J Physiol. 2004 Jun 15;557(Pt 3):829-41 - PubMed
  22. Neurosci Res. 2004 Feb;48(2):211-20 - PubMed
  23. J Neurosci. 1995 Oct;15(10):6890-904 - PubMed
  24. Eur J Neurosci. 2005 Dec;22(11):2708-22 - PubMed

Publication Types