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

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 KC...

Full description

Saved in:
Bibliographic Details
Published inClinical and experimental otorhinolaryngology Vol. 5; no. 3; pp. 117 - 121
Main Authors Suh, Myung-Whan, Ahn, Seung Cheol
Format Journal Article
LanguageEnglish
Published Korea (South) Korean Society of Otorhinolaryngology-Head and Neck Surgery 01.09.2012
대한이비인후과학회
Subjects
Online AccessGet full text
ISSN1976-8710
2005-0720
2005-0720
DOI10.3342/ceo.2012.5.3.117

Cover

Abstract 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. 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. 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). We concluded that weak expressions of KCC2 and NKCC1 in circling mice were due to partial destruction of cochleae.
AbstractList Objectives. From our previous study about the weak expressions of potassium-chloride (KCC2) and sodium-potassium-2chloride (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. KCI Citation Count: 0
ObjectivesFrom 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.MethodsRat 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.ResultsThe 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).ConclusionWe concluded that weak expressions of KCC2 and NKCC1 in circling mice were due to partial destruction of cochleae.
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.OBJECTIVESFrom 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.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.METHODSRat 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.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).RESULTSThe 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).We concluded that weak expressions of KCC2 and NKCC1 in circling mice were due to partial destruction of cochleae.CONCLUSIONWe concluded that weak expressions of KCC2 and NKCC1 in circling mice were due to partial destruction of cochleae.
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. 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. 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). We concluded that weak expressions of KCC2 and NKCC1 in circling mice were due to partial destruction of cochleae.
Author Suh, Myung-Whan
Ahn, Seung Cheol
AuthorAffiliation 1 Department of Otorhinolaryngology-Head & Neck Surgery, Dankook University College of Medicine, Cheonan, Korea
2 Department of Physiology, Dankook University College of Medicine, Cheonan, Korea
AuthorAffiliation_xml – name: 2 Department of Physiology, Dankook University College of Medicine, Cheonan, Korea
– name: 1 Department of Otorhinolaryngology-Head & Neck Surgery, Dankook University College of Medicine, Cheonan, Korea
Author_xml – sequence: 1
  givenname: Myung-Whan
  surname: Suh
  fullname: Suh, Myung-Whan
  organization: Department of Otorhinolaryngology-Head & Neck Surgery, Dankook University College of Medicine, Cheonan, Korea
– sequence: 2
  givenname: Seung Cheol
  surname: Ahn
  fullname: Ahn, Seung Cheol
  organization: Department of Physiology, Dankook University College of Medicine, Cheonan, Korea
BackLink https://www.ncbi.nlm.nih.gov/pubmed/22977707$$D View this record in MEDLINE/PubMed
https://www.kci.go.kr/kciportal/ci/sereArticleSearch/ciSereArtiView.kci?sereArticleSearchBean.artiId=ART001696025$$DAccess content in National Research Foundation of Korea (NRF)
BookMark eNp1UktvEzEQXqEi2gbunJCPIHWDH2t794JUhVfUqJVKOFte72zjdmOntjdS_wK_GicpFUXiNLbne4zG32lx5LyDonhL8JSxin404KcUEzrlUzYlRL4oTijGvMSS4qPihDRSlLUk-Lg4jfEWY8E5rl4Vx5Q2UkosT4pfn8EE0BE6NF-vR-fzxSS7tclCRL5HaQVothp8sB2gZdAubnxIEOIZupjNKNKuQ5f5RM6QdXv0Que2HtCPcQPB-oCuBrsFdAlj8G6veaGdXj8Y68qU7VL2vtYpvi5e9nqI8OaxToqfX78sZ9_LxdW3-ex8URpOm1SKridUSJCtoA2AlJwLDrpueC3rHhsJtOcMCK3zEgSTrGmEBqO5BkkEx2xSfDjoutCrO2OV13Zfb7y6C-r8ejlXhFbVjj0p5gds5_Wt2gS71uFhT9g_-HCjdEjWDKCAiKbtGeu5gKptRGNEq9tWVrKGmnc7308Hrc3YrqEz4FJe0zPR5x1nV3mmrWIVkxUhWeD9o0Dw9yPEpNY2GhgG7cCPURHMmrquZVVn6Lu_vZ5M_nx8BuADwAQfY4D-CUKw2mVL5WypXbYUV0zlbGWK-IdibNLJ-t20dvg_8Tdr9tOs
CitedBy_id crossref_primary_10_3389_fneur_2023_1207616
Cites_doi 10.1002/tera.1420290108
10.1523/JNEUROSCI.3002-08.2008
10.1007/BF00455127
10.1080/00016480600827071
10.1523/JNEUROSCI.15-10-06890.1995
10.1152/jn.1991.65.2.247
10.3342/ceo.2011.4.1.18
10.1016/j.bbrc.2010.12.129
10.1016/j.neures.2003.10.011
10.1152/jn.1998.80.5.2608
10.1111/j.1460-9568.2005.04465.x
10.3109/00016487909137180
10.1538/expanim.51.167
10.1523/JNEUROSCI.23-20-07516.2003
10.1002/(SICI)1097-4695(19971120)33:6<781::AID-NEU6>3.0.CO;2-5
10.1113/jphysiol.2004.062471
10.1113/jphysiol.1996.sp021505
10.1016/0378-5955(80)90032-5
10.1016/j.neures.2008.09.002
10.1038/16697
10.1523/JNEUROSCI.23-10-04134.2003
10.1016/0736-5748(90)90080-L
10.1523/JNEUROSCI.12-10-03935.1992
ContentType Journal Article
Copyright Copyright © 2012 by Korean Society of Otorhinolaryngology-Head and Neck Surgery. 2012
Copyright_xml – notice: Copyright © 2012 by Korean Society of Otorhinolaryngology-Head and Neck Surgery. 2012
DBID AAYXX
CITATION
NPM
7X8
5PM
DOA
ACYCR
DOI 10.3342/ceo.2012.5.3.117
DatabaseName CrossRef
PubMed
MEDLINE - Academic
PubMed Central (Full Participant titles)
DOAJ Directory of Open Access Journals
Korean Citation Index
DatabaseTitle CrossRef
PubMed
MEDLINE - Academic
DatabaseTitleList

MEDLINE - Academic
PubMed
Database_xml – sequence: 1
  dbid: DOA
  name: DOAJ Directory of Open Access Journals
  url: https://www.doaj.org/
  sourceTypes: Open Website
– sequence: 2
  dbid: NPM
  name: PubMed
  url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
  sourceTypes: Index Database
DeliveryMethod fulltext_linktorsrc
Discipline Medicine
EISSN 2005-0720
EndPage 121
ExternalDocumentID oai_kci_go_kr_ARTI_1244206
oai_doaj_org_article_e169bf33f56e4b969c6babb7478e85d0
PMC3437411
22977707
10_3342_ceo_2012_5_3_117
Genre Journal Article
GroupedDBID 29B
2WC
5-W
53G
5GY
8JR
8XY
9ZL
AAYXX
ACYCR
ADBBV
ADRAZ
AENEX
ALMA_UNASSIGNED_HOLDINGS
AOIJS
BAWUL
BCNDV
C1A
CITATION
CS3
DIK
DU5
E3Z
EF.
F5P
GROUPED_DOAJ
HYE
KQ8
M48
O5R
O5S
OK1
PGMZT
RNS
RPM
TR2
NPM
7X8
5PM
M~E
ID FETCH-LOGICAL-c529t-6df1267e7b629ee775565ea895878f0c7e2f53e1287206373996aeca5ae716503
IEDL.DBID M48
ISSN 1976-8710
2005-0720
IngestDate Tue Nov 21 21:47:12 EST 2023
Wed Aug 27 01:31:56 EDT 2025
Thu Aug 21 13:48:02 EDT 2025
Fri Jul 11 11:35:26 EDT 2025
Mon Jul 21 06:04:01 EDT 2025
Thu Apr 24 23:04:09 EDT 2025
Tue Jul 01 04:03:19 EDT 2025
IsDoiOpenAccess true
IsOpenAccess true
IsPeerReviewed true
IsScholarly true
Issue 3
Keywords Cochlea
Kanamycin
Lateral superior olive
NKCC1
KCC2
Language English
License http://creativecommons.org/licenses/by-nc/3.0
This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
LinkModel DirectLink
MergedId FETCHMERGED-LOGICAL-c529t-6df1267e7b629ee775565ea895878f0c7e2f53e1287206373996aeca5ae716503
Notes ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
G704-SER000001014.2012.5.3.009
OpenAccessLink http://journals.scholarsportal.info/openUrl.xqy?doi=10.3342/ceo.2012.5.3.117
PMID 22977707
PQID 1039888748
PQPubID 23479
PageCount 5
ParticipantIDs nrf_kci_oai_kci_go_kr_ARTI_1244206
doaj_primary_oai_doaj_org_article_e169bf33f56e4b969c6babb7478e85d0
pubmedcentral_primary_oai_pubmedcentral_nih_gov_3437411
proquest_miscellaneous_1039888748
pubmed_primary_22977707
crossref_primary_10_3342_ceo_2012_5_3_117
crossref_citationtrail_10_3342_ceo_2012_5_3_117
ProviderPackageCode CITATION
AAYXX
PublicationCentury 2000
PublicationDate 2012-09-01
PublicationDateYYYYMMDD 2012-09-01
PublicationDate_xml – month: 09
  year: 2012
  text: 2012-09-01
  day: 01
PublicationDecade 2010
PublicationPlace Korea (South)
PublicationPlace_xml – name: Korea (South)
PublicationTitle Clinical and experimental otorhinolaryngology
PublicationTitleAlternate Clin Exp Otorhinolaryngol
PublicationYear 2012
Publisher Korean Society of Otorhinolaryngology-Head and Neck Surgery
대한이비인후과학회
Publisher_xml – name: Korean Society of Otorhinolaryngology-Head and Neck Surgery
– name: 대한이비인후과학회
References Vale (10.3342/ceo.2012.5.3.117_ref23) 2003; 23
Chen (10.3342/ceo.2012.5.3.117_ref4) 1996; 494
Marot (10.3342/ceo.2012.5.3.117_ref16) 1980; 2
Luhmann (10.3342/ceo.2012.5.3.117_ref5) 1991; 65
Rivera (10.3342/ceo.2012.5.3.117_ref9) 1999; 397
Shibata (10.3342/ceo.2012.5.3.117_ref22) 2004; 48
Wu (10.3342/ceo.2012.5.3.117_ref7) 1992; 12
Cherubini (10.3342/ceo.2012.5.3.117_ref3) 1990; 8
Pradhan (10.3342/ceo.2012.5.3.117_ref11) 2011; 4
Lee (10.3342/ceo.2012.5.3.117_ref13) 2001; 51
Chung (10.3342/ceo.2012.5.3.117_ref12) 2007; 127
Lee (10.3342/ceo.2012.5.3.117_ref14) 2002; 51
Balakrishnan (10.3342/ceo.2012.5.3.117_ref21) 2003; 23
Singer (10.3342/ceo.2012.5.3.117_ref6) 1998; 80
Hong (10.3342/ceo.2012.5.3.117_ref20) 2008; 28
Lohrke (10.3342/ceo.2012.5.3.117_ref2) 2005; 22
Carlier (10.3342/ceo.2012.5.3.117_ref15) 1980; 226
Osako (10.3342/ceo.2012.5.3.117_ref18) 1979; 88
Lee (10.3342/ceo.2012.5.3.117_ref19) 2011; 405
Kitamura (10.3342/ceo.2012.5.3.117_ref24) 2008; 62
Plotkin (10.3342/ceo.2012.5.3.117_ref8) 1997; 33
Yamada (10.3342/ceo.2012.5.3.117_ref10) 2004; 557
Onejeme (10.3342/ceo.2012.5.3.117_ref17) 1984; 29
Kandler (10.3342/ceo.2012.5.3.117_ref1) 1995; 15
14741396 - Neurosci Res. 2004 Feb;48(2):211-20
15090604 - J Physiol. 2004 Jun 15;557(Pt 3):829-41
17364360 - Acta Otolaryngol. 2007 Mar;127(3):244-51
9819267 - J Neurophysiol. 1998 Nov;80(5):2608-20
12930790 - J Neurosci. 2003 Aug 20;23(20):7516-24
9369151 - J Neurobiol. 1997 Nov 20;33(6):781-95
9930699 - Nature. 1999 Jan 21;397(6716):251-5
21461058 - Clin Exp Otorhinolaryngol. 2011 Mar;4(1):18-23
19036993 - J Neurosci. 2008 Nov 26;28(48):13003-7
1403091 - J Neurosci. 1992 Oct;12(10):3935-45
8842004 - J Physiol. 1996 Jul 15;494 ( Pt 2):451-64
18840481 - Neurosci Res. 2008 Dec;62(4):270-7
532611 - Acta Otolaryngol. 1979;88(5-6):359-68
21215254 - Biochem Biophys Res Commun. 2011 Feb 11;405(2):162-7
1673153 - J Neurophysiol. 1991 Feb;65(2):247-63
2174638 - Int J Dev Neurosci. 1990;8(4):481-90
12764101 - J Neurosci. 2003 May 15;23(10):4134-45
16324105 - Eur J Neurosci. 2005 Dec;22(11):2708-22
7472446 - J Neurosci. 1995 Oct;15(10):6890-904
7364666 - Hear Res. 1980 Mar;2(2):111-3
11924819 - Comp Med. 2001 Dec;51(6):550-4
7458747 - Arch Otorhinolaryngol. 1980;226(3):129-33
6701807 - Teratology. 1984 Feb;29(1):57-71
12012726 - Exp Anim. 2002 Apr;51(2):167-71
References_xml – volume: 29
  start-page: 57
  issue: 1
  year: 1984
  ident: 10.3342/ceo.2012.5.3.117_ref17
  publication-title: Teratology
  doi: 10.1002/tera.1420290108
– volume: 28
  start-page: 13003
  issue: 48
  year: 2008
  ident: 10.3342/ceo.2012.5.3.117_ref20
  publication-title: J Neurosci
  doi: 10.1523/JNEUROSCI.3002-08.2008
– volume: 226
  start-page: 129
  issue: 3
  year: 1980
  ident: 10.3342/ceo.2012.5.3.117_ref15
  publication-title: Arch Otorhinolaryngol
  doi: 10.1007/BF00455127
– volume: 127
  start-page: 244
  issue: 3
  year: 2007
  ident: 10.3342/ceo.2012.5.3.117_ref12
  publication-title: Acta Otolaryngol
  doi: 10.1080/00016480600827071
– volume: 15
  start-page: 6890
  issue: 10
  year: 1995
  ident: 10.3342/ceo.2012.5.3.117_ref1
  publication-title: J Neurosci
  doi: 10.1523/JNEUROSCI.15-10-06890.1995
– volume: 65
  start-page: 247
  issue: 2
  year: 1991
  ident: 10.3342/ceo.2012.5.3.117_ref5
  publication-title: J Neurophysiol
  doi: 10.1152/jn.1991.65.2.247
– volume: 4
  start-page: 18
  issue: 1
  year: 2011
  ident: 10.3342/ceo.2012.5.3.117_ref11
  publication-title: Clin Exp Otorhinolaryngol
  doi: 10.3342/ceo.2011.4.1.18
– volume: 405
  start-page: 162
  issue: 2
  year: 2011
  ident: 10.3342/ceo.2012.5.3.117_ref19
  publication-title: Biochem Biophys Res Commun
  doi: 10.1016/j.bbrc.2010.12.129
– volume: 48
  start-page: 211
  issue: 2
  year: 2004
  ident: 10.3342/ceo.2012.5.3.117_ref22
  publication-title: Neurosci Res
  doi: 10.1016/j.neures.2003.10.011
– volume: 80
  start-page: 2608
  issue: 5
  year: 1998
  ident: 10.3342/ceo.2012.5.3.117_ref6
  publication-title: J Neurophysiol
  doi: 10.1152/jn.1998.80.5.2608
– volume: 22
  start-page: 2708
  issue: 11
  year: 2005
  ident: 10.3342/ceo.2012.5.3.117_ref2
  publication-title: Eur J Neurosci
  doi: 10.1111/j.1460-9568.2005.04465.x
– volume: 88
  start-page: 359
  issue: 5-6
  year: 1979
  ident: 10.3342/ceo.2012.5.3.117_ref18
  publication-title: Acta Otolaryngol
  doi: 10.3109/00016487909137180
– volume: 51
  start-page: 167
  issue: 2
  year: 2002
  ident: 10.3342/ceo.2012.5.3.117_ref14
  publication-title: Exp Anim
  doi: 10.1538/expanim.51.167
– volume: 23
  start-page: 7516
  issue: 20
  year: 2003
  ident: 10.3342/ceo.2012.5.3.117_ref23
  publication-title: J Neurosci
  doi: 10.1523/JNEUROSCI.23-20-07516.2003
– volume: 33
  start-page: 781
  issue: 6
  year: 1997
  ident: 10.3342/ceo.2012.5.3.117_ref8
  publication-title: J Neurobiol
  doi: 10.1002/(SICI)1097-4695(19971120)33:6<781::AID-NEU6>3.0.CO;2-5
– volume: 557
  start-page: 829
  issue: Pt 3
  year: 2004
  ident: 10.3342/ceo.2012.5.3.117_ref10
  publication-title: J Physiol
  doi: 10.1113/jphysiol.2004.062471
– volume: 494
  start-page: 451
  issue: Pt 2
  year: 1996
  ident: 10.3342/ceo.2012.5.3.117_ref4
  publication-title: J Physiol
  doi: 10.1113/jphysiol.1996.sp021505
– volume: 2
  start-page: 111
  issue: 2
  year: 1980
  ident: 10.3342/ceo.2012.5.3.117_ref16
  publication-title: Hear Res
  doi: 10.1016/0378-5955(80)90032-5
– volume: 62
  start-page: 270
  issue: 4
  year: 2008
  ident: 10.3342/ceo.2012.5.3.117_ref24
  publication-title: Neurosci Res
  doi: 10.1016/j.neures.2008.09.002
– volume: 397
  start-page: 251
  issue: 6716
  year: 1999
  ident: 10.3342/ceo.2012.5.3.117_ref9
  publication-title: Nature
  doi: 10.1038/16697
– volume: 23
  start-page: 4134
  issue: 10
  year: 2003
  ident: 10.3342/ceo.2012.5.3.117_ref21
  publication-title: J Neurosci
  doi: 10.1523/JNEUROSCI.23-10-04134.2003
– volume: 8
  start-page: 481
  issue: 4
  year: 1990
  ident: 10.3342/ceo.2012.5.3.117_ref3
  publication-title: Int J Dev Neurosci
  doi: 10.1016/0736-5748(90)90080-L
– volume: 12
  start-page: 3935
  issue: 10
  year: 1992
  ident: 10.3342/ceo.2012.5.3.117_ref7
  publication-title: J Neurosci
  doi: 10.1523/JNEUROSCI.12-10-03935.1992
– volume: 51
  start-page: 550
  issue: 6
  year: 2001
  ident: 10.3342/ceo.2012.5.3.117_ref13
  publication-title: Comp Med
– reference: 9930699 - Nature. 1999 Jan 21;397(6716):251-5
– reference: 9819267 - J Neurophysiol. 1998 Nov;80(5):2608-20
– reference: 21215254 - Biochem Biophys Res Commun. 2011 Feb 11;405(2):162-7
– reference: 21461058 - Clin Exp Otorhinolaryngol. 2011 Mar;4(1):18-23
– reference: 15090604 - J Physiol. 2004 Jun 15;557(Pt 3):829-41
– reference: 18840481 - Neurosci Res. 2008 Dec;62(4):270-7
– reference: 8842004 - J Physiol. 1996 Jul 15;494 ( Pt 2):451-64
– reference: 12930790 - J Neurosci. 2003 Aug 20;23(20):7516-24
– reference: 1403091 - J Neurosci. 1992 Oct;12(10):3935-45
– reference: 14741396 - Neurosci Res. 2004 Feb;48(2):211-20
– reference: 17364360 - Acta Otolaryngol. 2007 Mar;127(3):244-51
– reference: 532611 - Acta Otolaryngol. 1979;88(5-6):359-68
– reference: 7364666 - Hear Res. 1980 Mar;2(2):111-3
– reference: 12012726 - Exp Anim. 2002 Apr;51(2):167-71
– reference: 7458747 - Arch Otorhinolaryngol. 1980;226(3):129-33
– reference: 12764101 - J Neurosci. 2003 May 15;23(10):4134-45
– reference: 11924819 - Comp Med. 2001 Dec;51(6):550-4
– reference: 19036993 - J Neurosci. 2008 Nov 26;28(48):13003-7
– reference: 2174638 - Int J Dev Neurosci. 1990;8(4):481-90
– reference: 7472446 - J Neurosci. 1995 Oct;15(10):6890-904
– reference: 9369151 - J Neurobiol. 1997 Nov 20;33(6):781-95
– reference: 1673153 - J Neurophysiol. 1991 Feb;65(2):247-63
– reference: 6701807 - Teratology. 1984 Feb;29(1):57-71
– reference: 16324105 - Eur J Neurosci. 2005 Dec;22(11):2708-22
SSID ssj0065504
Score 1.8617433
Snippet From our previous study about the weak expressions of potassium-chloride (KCC2) and sodium-potassium-2 chloride (NKCC1) co-transporters in the lateral superior...
ObjectivesFrom our previous study about the weak expressions of potassium-chloride (KCC2) and sodium-potassium-2 chloride (NKCC1) co-transporters in the...
Objectives. From our previous study about the weak expressions of potassium-chloride (KCC2) and sodium-potassium-2chloride (NKCC1) co-transporters in the...
SourceID nrf
doaj
pubmedcentral
proquest
pubmed
crossref
SourceType Open Website
Open Access Repository
Aggregation Database
Index Database
Enrichment Source
StartPage 117
SubjectTerms Cochlea
Kanamycin
KCC2
Lateral superior olive
NKCC1
Original
이비인후과학
SummonAdditionalLinks – databaseName: DOAJ Directory of Open Access Journals
  dbid: DOA
  link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1Lb9QwELZQD4gL4k14ySAuSE3XsWM7PsJC1VJaJKBSb5ZfaVddHJTdPfAX-NWMnezSRQgunPKyk4k9Hn-jGX9G6KUzXongm5J7Xpd124hSOcdLYilpqVXVwLN9fCIOTuv3Z_zsylZfKSdsoAceGm4SKqFsy1jLRaitEsoJa6xNtO-h4T5760SRtTM12GABuHuIJ0sB470iQ4CSsZpOXF7zV9E9vsdSyHJrQsq8_TDNxL79E-T8PXPyylS0fwvdHDEkfj3IfhtdC_EOun48Rsnvoh9vMxZcBI8P0_KPDi5c3iUC3GLctRhAH55epNw7H_AvevN-sYuPplOKTfT4BM6qXTyLufQHk1Yqz_HnVWJG7nr8cQ5mEmdqj5jfeWSi-fodBChz7jp8-5NZLu6h0_13X6YH5bjnQuk4VctS-LaiQgZpBVUhSMkB8QXTKN7IpiVOBtpyFmBWkxTQjQR8I0xwhpsAnhcn7D7aiV0MDxGuG2OCUcpZD24IE8aTVta8MkFIsKqkQJN1w2s3EpKnfTHmGhyT1FUaukqnrtJcs8RKXqBXmxrfBjKOv5R9k_pyUy7RaOcboFx6VC79L-Uq0AvQBH3pZrl-Op53-rLX4Gwc6gSNoBEK9HytKBrGZgq4mBi61UKnMHsDVrxuCvRgUJyNPJQC8pYE5JRbKrUl8PaTOLvI_N-sZoADq0f_4w8foxup1YasuSdoZ9mvwlOAWUv7LI-on1nBJGg
  priority: 102
  providerName: Directory of Open Access Journals
Title Decreased Immunoreactivities of the Chloride Transporters, KCC2 and NKCC1, in the Lateral Superior Olive Neurons of Kanamycin-treated Rats
URI https://www.ncbi.nlm.nih.gov/pubmed/22977707
https://www.proquest.com/docview/1039888748
https://pubmed.ncbi.nlm.nih.gov/PMC3437411
https://doaj.org/article/e169bf33f56e4b969c6babb7478e85d0
https://www.kci.go.kr/kciportal/ci/sereArticleSearch/ciSereArtiView.kci?sereArticleSearchBean.artiId=ART001696025
Volume 5
hasFullText 1
inHoldings 1
isFullTextHit
isPrint
ispartofPNX Clinical and Experimental Otorhinolaryngology, 2012, 5(3), , pp.117-121
link http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfV1Lb9QwELagSIgL4t3wqAzigtRsE8eP-IAQLFQtZYsErNSb5ThOu-qSQHZXon-BX82Mk9120cIpLzux7LHnm4znG0JeOltq6cs8FqXgMa9yGWvnRJwULKlYodOOZ3t0LA_G_OOJOLkMj-47cLbRtMN8UuN2Ovj18-INTPjXaHFmnO25EMWXsoEYZOiEvE5ugF6SaIqN-MqnIAGL885RubEW0gIzQEMKM8te0VGByh80T91Wm1Do35spr2in_Tvkdg8r6dtODu6Sa76-R26Oesf5ffL7fYCHM1_SQ4wIaeDChcQRYCnTpqKAA-nwDLfjlZ5eMp63s116NBwyauuSHsNZuksndSj9yWLw8pR-XSBZctPSz1NYOWlg-6jDO49sbb9fQAPisJ0dvv3FzmcPyHj_w7fhQdynYYidYHoey7JKmVReFZJp75USAAK9zbXIVV4lTnlWicyDolMMAI8CyCOtd1ZYD8aYSLKHZKtuar9NKM-t9VZrV5RgmWTSlkmluEitlwoW2iQie8uON67nKMdUGVMDtgqOmoFRMzhqRpgMicoj8mpV40fHz_Gfsu9wLFflkFk73GjaU9NPVONTqYsqyyohPS-01E4WtigwzYDPBTbxBUiCOXeTUB-Pp405bw3YH4cG0RJ0QkSeLwXFwHRFH4ytfbOYGfS857Cw8zwijzrBWbVnKX4RUWsitdbg9Sf15CxQgmc8A2iYPv7nO5-QW9gV3e64p2Rr3i78M4BT82In_IbYCXPlD0nnHVU
linkProvider Scholars Portal
openUrl ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Decreased+Immunoreactivities+of+the+Chloride+Transporters%2C+KCC2+and+NKCC1%2C+in+the+Lateral+Superior+Olive+Neurons+of+Kanamycin-treated+Rats&rft.jtitle=Clinical+and+experimental+otorhinolaryngology&rft.au=Suh%2C+Myung-Whan&rft.au=Ahn%2C+Seung+Cheol&rft.date=2012-09-01&rft.eissn=2005-0720&rft.volume=5&rft.issue=3&rft.spage=117&rft_id=info:doi/10.3342%2Fceo.2012.5.3.117&rft_id=info%3Apmid%2F22977707&rft.externalDocID=22977707
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1976-8710&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1976-8710&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1976-8710&client=summon