The magnitudes of hyperpolarization-activated and low-voltage-activated potassium currents co-vary in neurons of the ventral cochlear nucleus

In the ventral cochlear nucleus (VCN), neurons have hyperpolarization-activated conductances, which in some cells are enormous, that contribute to the ability of neurons to convey acoustic information in the timing of their firing by decreasing the input resistance and speeding-up voltage changes. C...

Full description

Saved in:
Bibliographic Details
Published inJournal of neurophysiology Vol. 106; no. 2; pp. 630 - 640
Main Authors Cao, Xiao-Jie, Oertel, Donata
Format Journal Article
LanguageEnglish
Published United States American Physiological Society 01.08.2011
Subjects
Online AccessGet full text

Cover

Loading…
Abstract In the ventral cochlear nucleus (VCN), neurons have hyperpolarization-activated conductances, which in some cells are enormous, that contribute to the ability of neurons to convey acoustic information in the timing of their firing by decreasing the input resistance and speeding-up voltage changes. Comparisons of the electrophysiological properties of neurons in the VCN of mutant mice that lack the hyperpolarization-activated cyclic nucleotide-gated channel α subunit 1 (HCN1 −/− ) ( Nolan et al. 2003 ) with wild-type controls (HCN1 +/+ ) and with outbred ICR mice reveal that octopus, T stellate, and bushy cells maintain their electrophysiological distinctions in all strains. Hyperpolarization-activated (I h ) currents were smaller and slower, input resistances were higher, and membrane time constants were longer in HCN1 −/− than in HCN1 +/+ in octopus, bushy, and T stellate cells. There were significant differences in the average magnitudes of I h , input resistances, and time constants between HCN1 +/+ and ICR mice, but the resting potentials did not differ between strains. I h is opposed by a low-voltage-activated potassium (I KL ) current in bushy and octopus cells, whose magnitudes varied widely between neuronal types and between strains. The magnitudes of I h and I KL were correlated across neuronal types and across mouse strains. Furthermore, these currents balanced one another at the resting potential in individual cells. The magnitude of I h and I KL is linked in bushy and octopus cells and varies not only between HCN1 −/− and HCN1 +/+ but also between “wild-type” strains of mice, raising the question to what extent the wild-type strains reflect normal mice.
AbstractList In the ventral cochlear nucleus (VCN), neurons have hyperpolarization-activated conductances, which in some cells are enormous, that contribute to the ability of neurons to convey acoustic information in the timing of their firing by decreasing the input resistance and speeding-up voltage changes. Comparisons of the electrophysiological properties of neurons in the VCN of mutant mice that lack the hyperpolarization-activated cyclic nucleotide-gated channel α subunit 1 (HCN1 −/− ) ( Nolan et al. 2003 ) with wild-type controls (HCN1 +/+ ) and with outbred ICR mice reveal that octopus, T stellate, and bushy cells maintain their electrophysiological distinctions in all strains. Hyperpolarization-activated (I h ) currents were smaller and slower, input resistances were higher, and membrane time constants were longer in HCN1 −/− than in HCN1 +/+ in octopus, bushy, and T stellate cells. There were significant differences in the average magnitudes of I h , input resistances, and time constants between HCN1 +/+ and ICR mice, but the resting potentials did not differ between strains. I h is opposed by a low-voltage-activated potassium (I KL ) current in bushy and octopus cells, whose magnitudes varied widely between neuronal types and between strains. The magnitudes of I h and I KL were correlated across neuronal types and across mouse strains. Furthermore, these currents balanced one another at the resting potential in individual cells. The magnitude of I h and I KL is linked in bushy and octopus cells and varies not only between HCN1 −/− and HCN1 +/+ but also between “wild-type” strains of mice, raising the question to what extent the wild-type strains reflect normal mice.
In the ventral cochlear nucleus (VCN), neurons have hyperpolarization-activated conductances, which in some cells are enormous, that contribute to the ability of neurons to convey acoustic information in the timing of their firing by decreasing the input resistance and speeding-up voltage changes. Comparisons of the electrophysiological properties of neurons in the VCN of mutant mice that lack the hyperpolarization-activated cyclic nucleotide-gated channel α subunit 1 (HCN1(-/-)) (Nolan et al. 2003) with wild-type controls (HCN1(+/+)) and with outbred ICR mice reveal that octopus, T stellate, and bushy cells maintain their electrophysiological distinctions in all strains. Hyperpolarization-activated (I(h)) currents were smaller and slower, input resistances were higher, and membrane time constants were longer in HCN1(-/-) than in HCN1(+/+) in octopus, bushy, and T stellate cells. There were significant differences in the average magnitudes of I(h), input resistances, and time constants between HCN1(+/+) and ICR mice, but the resting potentials did not differ between strains. I(h) is opposed by a low-voltage-activated potassium (I(KL)) current in bushy and octopus cells, whose magnitudes varied widely between neuronal types and between strains. The magnitudes of I(h) and I(KL) were correlated across neuronal types and across mouse strains. Furthermore, these currents balanced one another at the resting potential in individual cells. The magnitude of I(h) and I(KL) is linked in bushy and octopus cells and varies not only between HCN1(-/-) and HCN1(+/+) but also between "wild-type" strains of mice, raising the question to what extent the wild-type strains reflect normal mice.
In the ventral cochlear nucleus (VCN), neurons have hyperpolarization-activated conductances, which in some cells are enormous, that contribute to the ability of neurons to convey acoustic information in the timing of their firing by decreasing the input resistance and speeding-up voltage changes. Comparisons of the electrophysiological properties of neurons in the VCN of mutant mice that lack the hyperpolarization-activated cyclic nucleotide-gated channel α subunit 1 (HCN1 −/− ) ( Nolan et al. 2003 ) with wild-type controls (HCN1 +/+ ) and with outbred ICR mice reveal that octopus, T stellate, and bushy cells maintain their electrophysiological distinctions in all strains. Hyperpolarization-activated (I h ) currents were smaller and slower, input resistances were higher, and membrane time constants were longer in HCN1 −/− than in HCN1 +/+ in octopus, bushy, and T stellate cells. There were significant differences in the average magnitudes of I h , input resistances, and time constants between HCN1 +/+ and ICR mice, but the resting potentials did not differ between strains. I h is opposed by a low-voltage-activated potassium (I KL ) current in bushy and octopus cells, whose magnitudes varied widely between neuronal types and between strains. The magnitudes of I h and I KL were correlated across neuronal types and across mouse strains. Furthermore, these currents balanced one another at the resting potential in individual cells. The magnitude of I h and I KL is linked in bushy and octopus cells and varies not only between HCN1 −/− and HCN1 +/+ but also between “wild-type” strains of mice, raising the question to what extent the wild-type strains reflect normal mice.
In the ventral cochlear nucleus (VCN), neurons have hyperpolarization-activated conductances, which in some cells are enormous, that contribute to the ability of neurons to convey acoustic information in the timing of their firing by decreasing the input resistance and speeding-up voltage changes. Comparisons of the electrophysiological properties of neurons in the VCN of mutant mice that lack the hyperpolarization-activated cyclic nucleotide-gated channel alpha subunit 1 (HCN1-/-) (Nolan et al. 2003) with wild-type controls (HCN1+/+) and with outbred ICR mice reveal that octopus, T stellate, and bushy cells maintain their electrophysiological distinctions in all strains. Hyperpolarization-activated (Ih) currents were smaller and slower, input resistances were higher, and membrane time constants were longer in HCN1-/- than in HCN1+/+ in octopus, bushy, and T stellate cells. There were significant differences in the average magnitudes of Ih, input resistances, and time constants between HCN1+/+ and ICR mice, but the resting potentials did not differ between strains. Ih is opposed by a low-voltage-activated potassium (IKL) current in bushy and octopus cells, whose magnitudes varied widely between neuronal types and between strains. The magnitudes of Ih and IKL were correlated across neuronal types and across mouse strains. Furthermore, these currents balanced one another at the resting potential in individual cells. The magnitude of Ih and IKL is linked in bushy and octopus cells and varies not only between HCN1-/- and HCN1+/+ but also between "wild-type" strains of mice, raising the question to what extent the wild-type strains reflect normal mice.
In the ventral cochlear nucleus (VCN), neurons have hyperpolarization-activated conductances, which in some cells are enormous, that contribute to the ability of neurons to convey acoustic information in the timing of their firing by decreasing the input resistance and speeding-up voltage changes. Comparisons of the electrophysiological properties of neurons in the VCN of mutant mice that lack the hyperpolarization-activated cyclic nucleotide-gated channel α subunit 1 (HCN1(-/-)) (Nolan et al. 2003) with wild-type controls (HCN1(+/+)) and with outbred ICR mice reveal that octopus, T stellate, and bushy cells maintain their electrophysiological distinctions in all strains. Hyperpolarization-activated (I(h)) currents were smaller and slower, input resistances were higher, and membrane time constants were longer in HCN1(-/-) than in HCN1(+/+) in octopus, bushy, and T stellate cells. There were significant differences in the average magnitudes of I(h), input resistances, and time constants between HCN1(+/+) and ICR mice, but the resting potentials did not differ between strains. I(h) is opposed by a low-voltage-activated potassium (I(KL)) current in bushy and octopus cells, whose magnitudes varied widely between neuronal types and between strains. The magnitudes of I(h) and I(KL) were correlated across neuronal types and across mouse strains. Furthermore, these currents balanced one another at the resting potential in individual cells. The magnitude of I(h) and I(KL) is linked in bushy and octopus cells and varies not only between HCN1(-/-) and HCN1(+/+) but also between "wild-type" strains of mice, raising the question to what extent the wild-type strains reflect normal mice.In the ventral cochlear nucleus (VCN), neurons have hyperpolarization-activated conductances, which in some cells are enormous, that contribute to the ability of neurons to convey acoustic information in the timing of their firing by decreasing the input resistance and speeding-up voltage changes. Comparisons of the electrophysiological properties of neurons in the VCN of mutant mice that lack the hyperpolarization-activated cyclic nucleotide-gated channel α subunit 1 (HCN1(-/-)) (Nolan et al. 2003) with wild-type controls (HCN1(+/+)) and with outbred ICR mice reveal that octopus, T stellate, and bushy cells maintain their electrophysiological distinctions in all strains. Hyperpolarization-activated (I(h)) currents were smaller and slower, input resistances were higher, and membrane time constants were longer in HCN1(-/-) than in HCN1(+/+) in octopus, bushy, and T stellate cells. There were significant differences in the average magnitudes of I(h), input resistances, and time constants between HCN1(+/+) and ICR mice, but the resting potentials did not differ between strains. I(h) is opposed by a low-voltage-activated potassium (I(KL)) current in bushy and octopus cells, whose magnitudes varied widely between neuronal types and between strains. The magnitudes of I(h) and I(KL) were correlated across neuronal types and across mouse strains. Furthermore, these currents balanced one another at the resting potential in individual cells. The magnitude of I(h) and I(KL) is linked in bushy and octopus cells and varies not only between HCN1(-/-) and HCN1(+/+) but also between "wild-type" strains of mice, raising the question to what extent the wild-type strains reflect normal mice.
Author Oertel, Donata
Cao, Xiao-Jie
Author_xml – sequence: 1
  givenname: Xiao-Jie
  surname: Cao
  fullname: Cao, Xiao-Jie
  organization: Department of Neuroscience, School of Neuroscience Medicine and Public Health, University of Wisconsin, Madison, Wisconsin
– sequence: 2
  givenname: Donata
  surname: Oertel
  fullname: Oertel, Donata
  organization: Department of Neuroscience, School of Neuroscience Medicine and Public Health, University of Wisconsin, Madison, Wisconsin
BackLink https://www.ncbi.nlm.nih.gov/pubmed/21562186$$D View this record in MEDLINE/PubMed
BookMark eNqFkk9v1DAQxS1URLeFI1fkG6cstpM49gUJVfyTKnEpZ2viOLteOXawnaDyHfjOuLstKgiJky2_3zw_zcwFOvPBG4ReUrKltGVvDn5LCKHtlhFKnqBNeWMVbaU4QxtCyr0mXXeOLlI6FK5rCXuGzhltOaOCb9DPm73BE-y8zctgEg4j3t_OJs7BQbQ_INvgK9DZrpDNgMEP2IXv1Rpchp15pMwhQ0p2mbBeYjQ-J6xDtUK8xdZjb5YY_NE-lw_XokdwhdB7ZyBiv2hnlvQcPR3BJfPi_rxEXz-8v7n6VF1_-fj56t11pRvR5Ep2YIZW6H40XNacNgODugfejKKXmndMiFrQUUJdGgGSj7p0aBxqIunQS87rS_T25Dsv_WQGfYqj5minElgFsOpPxdu92oVVFcNGkKYYvL43iOHbYlJWk03aOAfehCUpSToqKGv5f8kSteRitSzkq8ehfqd5GFYB6hOgY0gpmlFpm48TKhmtU5Sou5VQB6-OK6HuVqJUVX9VPRj_m_8FQ_a8Aw
CitedBy_id crossref_primary_10_1152_jn_00459_2018
crossref_primary_10_1038_s41598_018_38405_6
crossref_primary_10_1113_jphysiol_2012_229328
crossref_primary_10_1152_jn_01122_2011
crossref_primary_10_1152_jn_00234_2019
crossref_primary_10_1152_jn_00433_2012
crossref_primary_10_1152_jn_00435_2020
crossref_primary_10_3389_fncel_2016_00249
crossref_primary_10_1016_j_tins_2017_08_001
crossref_primary_10_1007_s10162_016_0610_8
crossref_primary_10_1007_s12576_015_0394_3
crossref_primary_10_1124_pr_117_014035
crossref_primary_10_1152_jn_00427_2011
crossref_primary_10_1152_jn_00660_2011
crossref_primary_10_1146_annurev_neuro_092920_121538
crossref_primary_10_1073_pnas_2203748119
crossref_primary_10_1523_JNEUROSCI_1811_18_2019
crossref_primary_10_1038_srep28584
crossref_primary_10_1371_journal_pone_0223137
crossref_primary_10_1016_j_heares_2015_06_014
crossref_primary_10_1113_JP275240
crossref_primary_10_1523_ENEURO_0166_22_2022
crossref_primary_10_1523_JNEUROSCI_2552_21_2022
crossref_primary_10_1074_jbc_M112_375832
crossref_primary_10_1113_jphysiol_2014_282194
crossref_primary_10_1085_jgp_201812031
crossref_primary_10_1111_ejn_12116
crossref_primary_10_1016_j_heares_2017_01_001
crossref_primary_10_1016_j_heares_2012_07_002
crossref_primary_10_1523_JNEUROSCI_5297_11_2012
crossref_primary_10_1038_s41467_024_55257_z
crossref_primary_10_1080_19336950_2017_1348870
crossref_primary_10_1152_jn_00523_2016
crossref_primary_10_1371_journal_pone_0085451
crossref_primary_10_3390_ijms23169260
crossref_primary_10_1007_s10162_016_0605_5
crossref_primary_10_1016_j_heares_2017_12_017
crossref_primary_10_1152_jn_00092_2012
crossref_primary_10_1523_JNEUROSCI_6500_11_2012
crossref_primary_10_3389_fnmol_2018_00183
crossref_primary_10_7554_eLife_83393
Cites_doi 10.1152/ajpcell.00389.2009
10.1113/jphysiol.2009.182873
10.1523/JNEUROSCI.21-18-07372.2001
10.1038/36103
10.1098/rspb.1993.0021
10.1111/j.1469-7793.2001.00733.x
10.1152/jn.1998.79.4.1755
10.1121/1.392494
10.1523/JNEUROSCI.1016-05.2005
10.1111/j.1460-9568.2005.04185.x
10.1152/jn.00624.2005
10.1038/nn.2735
10.1016/S0306-3623(96)00173-5
10.1523/JNEUROSCI.11-09-02865.1991
10.1113/jphysiol.2004.067421
10.1152/jn.00125.2002
10.1074/jbc.270.42.24776
10.1016/S0896-6273(00)80643-1
10.1016/S0026-895X(25)10594-4
10.1152/jn.01049.2004
10.1152/jn.1995.73.3.1043
10.1523/JNEUROSCI.0980-10.2010
10.1038/sj.bjp.0701004
10.1146/annurev.neuro.28.061604.135751
10.1152/jn.00052.2007
10.1152/jn.91300.2008
10.1152/jn.1999.81.6.2862
10.1016/j.heares.2006.02.006
10.1113/jphysiol.2002.027698
10.1523/JNEUROSCI.15-04-03138.1995
10.1002/cne.20407
10.1073/pnas.97.22.11773
10.1038/nn1639
10.1016/j.heares.2010.10.018
10.1016/j.neuroscience.2008.01.085
10.1523/JNEUROSCI.19-08-02897.1999
10.1016/S0022-3565(24)37521-4
10.1016/j.heares.2009.07.004
10.1152/jn.1990.63.5.1191
10.1523/JNEUROSCI.23-15-06357.2003
10.1523/JNEUROSCI.0740-10.2010
10.1152/jn.00587.2001
10.1002/cne.11039
10.1016/S0026-895X(25)13197-0
10.1038/nn.2530
10.1523/JNEUROSCI.04-06-01577.1984
10.1152/jn.2001.86.5.2299
10.1046/j.1432-1327.2001.02036.x
10.1152/jn.1998.79.1.51
10.1002/cne.902950112
10.1016/0014-5793(96)00211-6
10.1046/j.1432-1327.1999.00493.x
10.1111/j.1460-9568.2009.06925.x
10.1152/jn.2000.84.2.806
10.1073/pnas.0813058106
10.1038/31255
10.1152/jn.00582.2006
10.1152/jn.00385.2006
10.1152/jn.1993.70.4.1420
10.1074/jbc.C000738200
10.1523/JNEUROSCI.1738-07.2007
10.1111/j.0953-816X.2003.03133.x
10.1002/cne.903600110
10.1016/j.neuron.2008.10.020
10.1515/BC.1999.121
10.1146/annurev.physiol.65.092101.142734
10.1007/978-1-4757-3654-0_4
10.1016/S0092-8674(00)81434-8
10.1113/jphysiol.2006.114702
10.1007/BF02110698
10.1111/j.0953-816X.2004.03456.x
10.1074/jbc.M610978200
10.1152/jn.1997.78.6.3019
10.1016/S0092-8674(03)00884-5
ContentType Journal Article
Copyright Copyright © 2011 the American Physiological Society 2011
Copyright_xml – notice: Copyright © 2011 the American Physiological Society 2011
DBID AAYXX
CITATION
CGR
CUY
CVF
ECM
EIF
NPM
7X8
7TK
7TN
F1W
H95
L.G
5PM
DOI 10.1152/jn.00015.2010
DatabaseName CrossRef
Medline
MEDLINE
MEDLINE (Ovid)
MEDLINE
MEDLINE
PubMed
MEDLINE - Academic
Neurosciences Abstracts
Oceanic Abstracts
ASFA: Aquatic Sciences and Fisheries Abstracts
Aquatic Science & Fisheries Abstracts (ASFA) 1: Biological Sciences & Living Resources
Aquatic Science & Fisheries Abstracts (ASFA) Professional
PubMed Central (Full Participant titles)
DatabaseTitle CrossRef
MEDLINE
Medline Complete
MEDLINE with Full Text
PubMed
MEDLINE (Ovid)
MEDLINE - Academic
Aquatic Science & Fisheries Abstracts (ASFA) Professional
Oceanic Abstracts
Aquatic Science & Fisheries Abstracts (ASFA) 1: Biological Sciences & Living Resources
Neurosciences Abstracts
ASFA: Aquatic Sciences and Fisheries Abstracts
DatabaseTitleList
MEDLINE
CrossRef
Aquatic Science & Fisheries Abstracts (ASFA) Professional
MEDLINE - Academic
Database_xml – sequence: 1
  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
– sequence: 2
  dbid: EIF
  name: MEDLINE
  url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search
  sourceTypes: Index Database
DeliveryMethod fulltext_linktorsrc
Discipline Anatomy & Physiology
EISSN 1522-1598
EndPage 640
ExternalDocumentID PMC3154804
21562186
10_1152_jn_00015_2010
Genre Journal Article
Comparative Study
Research Support, N.I.H., Extramural
GrantInformation_xml – fundername: NIDCD NIH HHS
  grantid: DC00176
– fundername: NIDCD NIH HHS
  grantid: R01 DC000176
GroupedDBID ---
-DZ
-~X
.55
.GJ
0VX
18M
1CY
1Z7
29L
2WC
39C
3O-
4.4
41~
53G
5GY
5VS
8M5
AAYXX
ABCQX
ABHWK
ABIVO
ABJNI
ABKWE
ACGFO
ACGFS
ACNCT
ADBBV
ADFNX
ADHGD
ADIYS
AENEX
AETEA
AFFNX
AFOSN
AI.
AIZAD
ALMA_UNASSIGNED_HOLDINGS
BAWUL
BKKCC
BTFSW
C1A
CITATION
CS3
DIK
DU5
E3Z
EBS
EJD
EMOBN
F5P
H13
H~9
ITBOX
KQ8
L7B
MVM
NEJ
OHT
OK1
P2P
RAP
RHI
RPL
RPRKH
SJN
TR2
UHB
UPT
UQL
VH1
W8F
WH7
WOQ
WOW
X7M
XJT
XOL
XSW
YBH
YQT
YSK
ZGI
ZXP
ZY4
CGR
CUY
CVF
ECM
EIF
NPM
7X8
7TK
7TN
F1W
H95
L.G
5PM
ID FETCH-LOGICAL-c484t-97aed58cbfe693614d2a3ba64f8b9c67288381f9a3159a96fc001fd3091db9663
ISSN 0022-3077
1522-1598
IngestDate Thu Aug 21 18:24:46 EDT 2025
Thu Jul 10 18:04:19 EDT 2025
Fri Jul 11 00:58:38 EDT 2025
Mon Jul 21 05:54:55 EDT 2025
Thu Apr 24 22:55:33 EDT 2025
Tue Jul 01 05:21:42 EDT 2025
IsDoiOpenAccess false
IsOpenAccess true
IsPeerReviewed true
IsScholarly true
Issue 2
Language English
LinkModel OpenURL
MergedId FETCHMERGED-LOGICAL-c484t-97aed58cbfe693614d2a3ba64f8b9c67288381f9a3159a96fc001fd3091db9663
Notes ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-1
content type line 23
ObjectType-Article-1
ObjectType-Feature-2
OpenAccessLink https://www.ncbi.nlm.nih.gov/pmc/articles/3154804
PMID 21562186
PQID 883309239
PQPubID 23479
PageCount 11
ParticipantIDs pubmedcentral_primary_oai_pubmedcentral_nih_gov_3154804
proquest_miscellaneous_907181256
proquest_miscellaneous_883309239
pubmed_primary_21562186
crossref_citationtrail_10_1152_jn_00015_2010
crossref_primary_10_1152_jn_00015_2010
ProviderPackageCode CITATION
AAYXX
PublicationCentury 2000
PublicationDate 2011-08-01
PublicationDateYYYYMMDD 2011-08-01
PublicationDate_xml – month: 08
  year: 2011
  text: 2011-08-01
  day: 01
PublicationDecade 2010
PublicationPlace United States
PublicationPlace_xml – name: United States
– name: Bethesda, MD
PublicationTitle Journal of neurophysiology
PublicationTitleAlternate J Neurophysiol
PublicationYear 2011
Publisher American Physiological Society
Publisher_xml – name: American Physiological Society
References B20
B64
B21
B65
B22
B66
B67
B24
B68
B25
B69
B26
B27
B29
B71
B72
B73
B30
B74
B31
B75
B32
B33
B34
B35
B36
B37
B38
B39
Hopkins WF (B28) 1998; 285
B2
B3
B4
B5
B6
B7
B8
Adams JC (B1) 1997; 3
B9
B40
B41
B42
B43
B44
B45
B46
Werkman TR (B70) 1993; 44
B47
B48
B49
Grissmer S (B23) 1994; 45
B50
B51
B52
B53
B10
B54
B11
B55
B12
B56
B13
B57
B14
B58
B15
B59
B16
B17
B18
B19
B60
B61
B62
B63
14651847 - Cell. 2003 Nov 26;115(5):551-64
8355670 - Mol Pharmacol. 1993 Aug;44(2):430-6
20610748 - J Neurosci. 2010 Jul 7;30(27):9145-56
2993393 - J Acoust Soc Am. 1985 Jul;78(1 Pt 2):328-33
15235085 - J Physiol. 2004 Aug 15;559(Pt 1):25-33
2341631 - J Comp Neurol. 1990 May 1;295(1):136-54
7506755 - J Neurophysiol. 1993 Oct;70(4):1420-32
19788576 - Eur J Neurosci. 2009 Oct;30(7):1227-38
16029204 - Eur J Neurosci. 2005 Jul;22(1):147-57
12783951 - J Neurophysiol. 2003 Jun;89(6):3070-82
17553794 - J Biol Chem. 2007 Aug 3;282(31):22900-9
18995822 - Neuron. 2008 Nov 6;60(3):477-82
11698520 - J Neurophysiol. 2001 Nov;86(5):2299-311
11483704 - J Physiol. 2001 Aug 1;534(Pt 3):733-44
16135745 - J Neurosci. 2005 Aug 31;25(35):7887-95
1880553 - J Neurosci. 1991 Sep;11(9):2865-80
16807346 - J Neurophysiol. 2006 Oct;96(4):1860-76
9634236 - Nature. 1998 Jun 11;393(6685):587-91
9630217 - Cell. 1998 May 29;93(5):717-29
16647828 - Hear Res. 2006 Jun-Jul;216-217:52-63
9425176 - J Neurophysiol. 1998 Jan;79(1):51-63
14725627 - Eur J Neurosci. 2004 Jan;19(2):325-33
9134213 - Br J Pharmacol. 1997 Mar;120(6):1029-34
21270780 - Nat Neurosci. 2011 Feb;14(2):133-8
19346492 - Proc Natl Acad Sci U S A. 2009 Apr 21;106(16):6760-5
11976365 - J Neurophysiol. 2002 May;87(5):2262-70
18424000 - Neuroscience. 2008 Jun 12;154(1):77-86
8096080 - Proc Biol Sci. 1993 Feb 22;251(1331):143-50
15800074 - J Neurophysiol. 2005 Jul;94(1):821-32
16444270 - Nat Neurosci. 2006 Mar;9(3):356-62
14991560 - J Comp Neurol. 2004 Apr 5;471(3):241-76
20364143 - Nat Neurosci. 2010 May;13(5):601-9
9535945 - J Neurophysiol. 1998 Apr;79(4):1755-67
6726347 - J Neurosci. 1984 Jun;4(6):1577-88
20130205 - Am J Physiol Cell Physiol. 2010 May;298(5):C1066-76
11549747 - J Neurosci. 2001 Sep 15;21(18):7372-83
12867521 - J Neurosci. 2003 Jul 16;23(15):6357-61
19403742 - J Neurophysiol. 2009 Jul;102(1):167-80
15245481 - Eur J Neurosci. 2004 Jul;20(1):79-91
11133998 - J Biol Chem. 2001 Mar 2;276(9):6069-72
11050208 - Proc Natl Acad Sci U S A. 2000 Oct 24;97(22):11773-9
19615433 - Hear Res. 2009 Oct;256(1-2):93-103
20100739 - J Physiol. 2010 Mar 15;588(Pt 6):923-38
2358869 - J Neurophysiol. 1990 May;63(5):1191-212
11248683 - Eur J Biochem. 2001 Mar;268(6):1646-52
10429208 - Eur J Biochem. 1999 Jul;263(1):230-7
12702747 - J Physiol. 2003 Jun 1;549(Pt 2):347-59
8612784 - FEBS Lett. 1996 Mar 25;383(1-2):26-30
8807399 - J Bioenerg Biomembr. 1996 Jun;28(3):231-53
16776588 - Annu Rev Neurosci. 2006;29:307-23
7517498 - Mol Pharmacol. 1994 Jun;45(6):1227-34
16916913 - J Physiol. 2006 Nov 1;576(Pt 3):849-64
17670973 - J Neurosci. 2007 Aug 1;27(31):8268-77
9618407 - J Pharmacol Exp Ther. 1998 Jun;285(3):1051-60
12471170 - Annu Rev Physiol. 2003;65:453-80
10191307 - J Neurosci. 1999 Apr 15;19(8):2897-905
20861392 - J Neurosci. 2010 Sep 22;30(38):12885-95
7608754 - J Neurophysiol. 1995 Mar;73(3):1043-62
7559595 - J Biol Chem. 1995 Oct 20;270(42):24776-81
16192334 - J Neurophysiol. 2006 Jan;95(1):76-87
16943313 - J Neurophysiol. 2006 Dec;96(6):2857-67
10938307 - J Neurophysiol. 2000 Aug;84(2):806-17
10494850 - Biol Chem. 1999 Jul-Aug;380(7-8):975-80
15669051 - J Comp Neurol. 2005 Feb 21;482(4):349-71
17428908 - J Neurophysiol. 2007 Jun;97(6):3961-75
9405521 - J Neurophysiol. 1997 Dec;78(6):3019-27
9495341 - Nature. 1998 Feb 26;391(6670):892-6
21056098 - Hear Res. 2011 Jun;276(1-2):61-9
9883717 - Neuron. 1998 Dec;21(6):1235-8
10368403 - J Neurophysiol. 1999 Jun;81(6):2862-74
7499559 - J Comp Neurol. 1995 Sep 11;360(1):135-49
9112070 - Gen Pharmacol. 1997 Jan;28(1):7-12
7722652 - J Neurosci. 1995 Apr;15(4):3138-53
References_xml – ident: B27
  doi: 10.1152/ajpcell.00389.2009
– ident: B32
  doi: 10.1113/jphysiol.2009.182873
– ident: B18
  doi: 10.1523/JNEUROSCI.21-18-07372.2001
– ident: B66
  doi: 10.1038/36103
– ident: B17
  doi: 10.1098/rspb.1993.0021
– ident: B12
  doi: 10.1111/j.1469-7793.2001.00733.x
– ident: B40
  doi: 10.1152/jn.1998.79.4.1755
– ident: B49
  doi: 10.1121/1.392494
– ident: B64
  doi: 10.1523/JNEUROSCI.1016-05.2005
– ident: B35
  doi: 10.1111/j.1460-9568.2005.04185.x
– ident: B59
  doi: 10.1152/jn.00624.2005
– ident: B38
  doi: 10.1038/nn.2735
– ident: B25
  doi: 10.1016/S0306-3623(96)00173-5
– ident: B37
  doi: 10.1523/JNEUROSCI.11-09-02865.1991
– ident: B34
  doi: 10.1113/jphysiol.2004.067421
– ident: B60
  doi: 10.1152/jn.00125.2002
– ident: B67
  doi: 10.1074/jbc.270.42.24776
– ident: B29
  doi: 10.1016/S0896-6273(00)80643-1
– volume: 45
  start-page: 1227
  year: 1994
  ident: B23
  publication-title: Mol Pharmacol
  doi: 10.1016/S0026-895X(25)10594-4
– ident: B9
  doi: 10.1152/jn.01049.2004
– ident: B30
  doi: 10.1152/jn.1995.73.3.1043
– ident: B22
  doi: 10.1523/JNEUROSCI.0980-10.2010
– ident: B55
  doi: 10.1038/sj.bjp.0701004
– ident: B13
  doi: 10.1146/annurev.neuro.28.061604.135751
– ident: B10
  doi: 10.1152/jn.00052.2007
– ident: B19
  doi: 10.1152/jn.91300.2008
– ident: B73
  doi: 10.1152/jn.1999.81.6.2862
– ident: B41
  doi: 10.1016/j.heares.2006.02.006
– ident: B2
  doi: 10.1113/jphysiol.2002.027698
– ident: B21
  doi: 10.1523/JNEUROSCI.15-04-03138.1995
– ident: B65
  doi: 10.1002/cne.20407
– ident: B50
  doi: 10.1073/pnas.97.22.11773
– ident: B63
  doi: 10.1038/nn1639
– ident: B52
  doi: 10.1016/j.heares.2010.10.018
– ident: B51
  doi: 10.1016/j.neuroscience.2008.01.085
– ident: B20
  doi: 10.1523/JNEUROSCI.19-08-02897.1999
– volume: 285
  start-page: 1051
  year: 1998
  ident: B28
  publication-title: J Pharmacol Exp Ther
  doi: 10.1016/S0022-3565(24)37521-4
– ident: B3
  doi: 10.1016/j.heares.2009.07.004
– ident: B8
  doi: 10.1152/jn.1990.63.5.1191
– ident: B45
  doi: 10.1523/JNEUROSCI.23-15-06357.2003
– ident: B11
  doi: 10.1523/JNEUROSCI.0740-10.2010
– ident: B16
  doi: 10.1152/jn.00587.2001
– ident: B48
  doi: 10.1002/cne.11039
– volume: 44
  start-page: 430
  year: 1993
  ident: B70
  publication-title: Mol Pharmacol
  doi: 10.1016/S0026-895X(25)13197-0
– ident: B39
  doi: 10.1038/nn.2530
– ident: B74
  doi: 10.1523/JNEUROSCI.04-06-01577.1984
– ident: B5
  doi: 10.1152/jn.2001.86.5.2299
– ident: B44
  doi: 10.1046/j.1432-1327.2001.02036.x
– ident: B15
  doi: 10.1152/jn.1998.79.1.51
– ident: B53
  doi: 10.1002/cne.902950112
– ident: B57
  doi: 10.1016/0014-5793(96)00211-6
– ident: B69
  doi: 10.1046/j.1432-1327.1999.00493.x
– ident: B26
  doi: 10.1111/j.1460-9568.2009.06925.x
– ident: B4
  doi: 10.1152/jn.2000.84.2.806
– volume: 3
  start-page: 335
  year: 1997
  ident: B1
  publication-title: Auditory Neurosci
– ident: B72
  doi: 10.1073/pnas.0813058106
– ident: B36
  doi: 10.1038/31255
– ident: B54
  doi: 10.1152/jn.00582.2006
– ident: B24
  doi: 10.1152/jn.00385.2006
– ident: B6
  doi: 10.1152/jn.1993.70.4.1420
– ident: B68
  doi: 10.1074/jbc.C000738200
– ident: B56
  doi: 10.1523/JNEUROSCI.1738-07.2007
– ident: B7
  doi: 10.1111/j.0953-816X.2003.03133.x
– ident: B62
  doi: 10.1002/cne.903600110
– ident: B46
  doi: 10.1016/j.neuron.2008.10.020
– ident: B43
  doi: 10.1515/BC.1999.121
– ident: B58
  doi: 10.1146/annurev.physiol.65.092101.142734
– ident: B75
  doi: 10.1007/978-1-4757-3654-0_4
– ident: B61
  doi: 10.1016/S0092-8674(00)81434-8
– ident: B33
  doi: 10.1113/jphysiol.2006.114702
– ident: B14
  doi: 10.1007/BF02110698
– ident: B31
  doi: 10.1111/j.0953-816X.2004.03456.x
– ident: B71
  doi: 10.1074/jbc.M610978200
– ident: B42
  doi: 10.1152/jn.1997.78.6.3019
– ident: B47
  doi: 10.1016/S0092-8674(03)00884-5
– reference: 20100739 - J Physiol. 2010 Mar 15;588(Pt 6):923-38
– reference: 11698520 - J Neurophysiol. 2001 Nov;86(5):2299-311
– reference: 18995822 - Neuron. 2008 Nov 6;60(3):477-82
– reference: 11483704 - J Physiol. 2001 Aug 1;534(Pt 3):733-44
– reference: 9634236 - Nature. 1998 Jun 11;393(6685):587-91
– reference: 12471170 - Annu Rev Physiol. 2003;65:453-80
– reference: 19788576 - Eur J Neurosci. 2009 Oct;30(7):1227-38
– reference: 14725627 - Eur J Neurosci. 2004 Jan;19(2):325-33
– reference: 20364143 - Nat Neurosci. 2010 May;13(5):601-9
– reference: 15800074 - J Neurophysiol. 2005 Jul;94(1):821-32
– reference: 7499559 - J Comp Neurol. 1995 Sep 11;360(1):135-49
– reference: 19346492 - Proc Natl Acad Sci U S A. 2009 Apr 21;106(16):6760-5
– reference: 14991560 - J Comp Neurol. 2004 Apr 5;471(3):241-76
– reference: 15669051 - J Comp Neurol. 2005 Feb 21;482(4):349-71
– reference: 16916913 - J Physiol. 2006 Nov 1;576(Pt 3):849-64
– reference: 15245481 - Eur J Neurosci. 2004 Jul;20(1):79-91
– reference: 7722652 - J Neurosci. 1995 Apr;15(4):3138-53
– reference: 16192334 - J Neurophysiol. 2006 Jan;95(1):76-87
– reference: 11248683 - Eur J Biochem. 2001 Mar;268(6):1646-52
– reference: 15235085 - J Physiol. 2004 Aug 15;559(Pt 1):25-33
– reference: 16776588 - Annu Rev Neurosci. 2006;29:307-23
– reference: 2993393 - J Acoust Soc Am. 1985 Jul;78(1 Pt 2):328-33
– reference: 9618407 - J Pharmacol Exp Ther. 1998 Jun;285(3):1051-60
– reference: 16444270 - Nat Neurosci. 2006 Mar;9(3):356-62
– reference: 11976365 - J Neurophysiol. 2002 May;87(5):2262-70
– reference: 10368403 - J Neurophysiol. 1999 Jun;81(6):2862-74
– reference: 8807399 - J Bioenerg Biomembr. 1996 Jun;28(3):231-53
– reference: 10429208 - Eur J Biochem. 1999 Jul;263(1):230-7
– reference: 16807346 - J Neurophysiol. 2006 Oct;96(4):1860-76
– reference: 21056098 - Hear Res. 2011 Jun;276(1-2):61-9
– reference: 12783951 - J Neurophysiol. 2003 Jun;89(6):3070-82
– reference: 19615433 - Hear Res. 2009 Oct;256(1-2):93-103
– reference: 8096080 - Proc Biol Sci. 1993 Feb 22;251(1331):143-50
– reference: 9883717 - Neuron. 1998 Dec;21(6):1235-8
– reference: 11050208 - Proc Natl Acad Sci U S A. 2000 Oct 24;97(22):11773-9
– reference: 16029204 - Eur J Neurosci. 2005 Jul;22(1):147-57
– reference: 16135745 - J Neurosci. 2005 Aug 31;25(35):7887-95
– reference: 8612784 - FEBS Lett. 1996 Mar 25;383(1-2):26-30
– reference: 9112070 - Gen Pharmacol. 1997 Jan;28(1):7-12
– reference: 10938307 - J Neurophysiol. 2000 Aug;84(2):806-17
– reference: 1880553 - J Neurosci. 1991 Sep;11(9):2865-80
– reference: 18424000 - Neuroscience. 2008 Jun 12;154(1):77-86
– reference: 12867521 - J Neurosci. 2003 Jul 16;23(15):6357-61
– reference: 20130205 - Am J Physiol Cell Physiol. 2010 May;298(5):C1066-76
– reference: 7559595 - J Biol Chem. 1995 Oct 20;270(42):24776-81
– reference: 10494850 - Biol Chem. 1999 Jul-Aug;380(7-8):975-80
– reference: 12702747 - J Physiol. 2003 Jun 1;549(Pt 2):347-59
– reference: 9134213 - Br J Pharmacol. 1997 Mar;120(6):1029-34
– reference: 7506755 - J Neurophysiol. 1993 Oct;70(4):1420-32
– reference: 21270780 - Nat Neurosci. 2011 Feb;14(2):133-8
– reference: 7517498 - Mol Pharmacol. 1994 Jun;45(6):1227-34
– reference: 20610748 - J Neurosci. 2010 Jul 7;30(27):9145-56
– reference: 9425176 - J Neurophysiol. 1998 Jan;79(1):51-63
– reference: 16943313 - J Neurophysiol. 2006 Dec;96(6):2857-67
– reference: 7608754 - J Neurophysiol. 1995 Mar;73(3):1043-62
– reference: 17553794 - J Biol Chem. 2007 Aug 3;282(31):22900-9
– reference: 9630217 - Cell. 1998 May 29;93(5):717-29
– reference: 9535945 - J Neurophysiol. 1998 Apr;79(4):1755-67
– reference: 16647828 - Hear Res. 2006 Jun-Jul;216-217:52-63
– reference: 20861392 - J Neurosci. 2010 Sep 22;30(38):12885-95
– reference: 11133998 - J Biol Chem. 2001 Mar 2;276(9):6069-72
– reference: 8355670 - Mol Pharmacol. 1993 Aug;44(2):430-6
– reference: 6726347 - J Neurosci. 1984 Jun;4(6):1577-88
– reference: 14651847 - Cell. 2003 Nov 26;115(5):551-64
– reference: 17428908 - J Neurophysiol. 2007 Jun;97(6):3961-75
– reference: 17670973 - J Neurosci. 2007 Aug 1;27(31):8268-77
– reference: 10191307 - J Neurosci. 1999 Apr 15;19(8):2897-905
– reference: 2341631 - J Comp Neurol. 1990 May 1;295(1):136-54
– reference: 11549747 - J Neurosci. 2001 Sep 15;21(18):7372-83
– reference: 2358869 - J Neurophysiol. 1990 May;63(5):1191-212
– reference: 19403742 - J Neurophysiol. 2009 Jul;102(1):167-80
– reference: 9405521 - J Neurophysiol. 1997 Dec;78(6):3019-27
– reference: 9495341 - Nature. 1998 Feb 26;391(6670):892-6
SSID ssj0007502
Score 2.2383494
Snippet In the ventral cochlear nucleus (VCN), neurons have hyperpolarization-activated conductances, which in some cells are enormous, that contribute to the ability...
SourceID pubmedcentral
proquest
pubmed
crossref
SourceType Open Access Repository
Aggregation Database
Index Database
Enrichment Source
StartPage 630
SubjectTerms Animals
Cochlear Nucleus - cytology
Cochlear Nucleus - physiology
Cyclic Nucleotide-Gated Cation Channels - deficiency
Cyclic Nucleotide-Gated Cation Channels - physiology
Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels
Membrane Potentials - genetics
Mice
Mice, 129 Strain
Mice, Inbred C57BL
Mice, Inbred ICR
Mice, Knockout
Mice, Transgenic
Neural Inhibition - genetics
Neurons - classification
Neurons - physiology
Octopus
Potassium Channels - deficiency
Potassium Channels - genetics
Potassium Channels - physiology
Species Specificity
Title The magnitudes of hyperpolarization-activated and low-voltage-activated potassium currents co-vary in neurons of the ventral cochlear nucleus
URI https://www.ncbi.nlm.nih.gov/pubmed/21562186
https://www.proquest.com/docview/883309239
https://www.proquest.com/docview/907181256
https://pubmed.ncbi.nlm.nih.gov/PMC3154804
Volume 106
hasFullText 1
inHoldings 1
isFullTextHit
isPrint
link http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1Lb9NAEF5F5cIFAeWR8tAeUC9hS-LH2nusIlBVVChSK-Vmrddr1VVjR6kTVP4DP4X_yMzu2rFJi6AXK7LXtuL5PPvNePYbQt4FOs-DWGmG4mwsyMYRk56vWARbmC91LCe4OPnkCz86D45n4Www-NWpWlrV6YH6ceu6kvtYFfaBXXGV7H9Ytr0o7IDfYF_YgoVh-882nkus_1llVjz2AsLK5QLDVbe-kuHChbVEXokp8qvqOwOHVIMX6RxZVDVw6GI1Hykr13Q9UhVbY0FdUY6M5KWtlkOWurb5YBihLrDnxKhESWSXP9imueZskz_pJfCn0uRoZ4Ws2HHRouurXta2bgCT1rXsJiVslrVb4NF8bTptLm8Q5wpRu_4Y1xKMXSMX7Vww7AOSFfd89Jh3wOh1PC53n3Xs5M2t9tP2vBCizuxleWDWjpuKvu44MOtibkACDIhjm67N9NgWLZ6eTH0M8FB99oEHUQm61c_fNuL0QL424vTwpxpJ19D70LuzEaC2t-mzoa0Q589K3Q71OXtMHjlj0kMLwCdkoMunZPcQ7FPNb-g-bR__zS75CZikG0zSKqd_wSQFTNJbMUlbTNIGk9RhkhYldZjEywMmqcMkbTBJHSafkfNPH8-mR8y1_GAqiIOaiUjqLIxVmmsufKCOmSf9VPIgj1OheIS9seNJLiRYQkjBcwVPNc98YL1ZCpG7_5zslFWpXxLKRZ5OlOBRmqsAAm8RaoiOJjE2GIBJVQzJ--bRJ8rp4WNblqvExMWhl1yWpjQjTNBoQ7LfDl9YIZi7BtLGjgm4avz-Jktdra4T7Os9hoBK3D1EAOMHyh3yIXlhLd_erIHMkEQ9TLQDUCi-f6QsLoxgvIPt3r3PfEUebt7y12SnXq70GyDjdfrWvAK_AfGe6YA
linkProvider Colorado Alliance of Research Libraries
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=The+magnitudes+of+hyperpolarization-activated+and+low-voltage-activated+potassium+currents+co-vary+in+neurons+of+the+ventral+cochlear+nucleus&rft.jtitle=Journal+of+neurophysiology&rft.au=Cao%2C+Xiao-Jie&rft.au=Oertel%2C+Donata&rft.date=2011-08-01&rft.pub=American+Physiological+Society&rft.issn=0022-3077&rft.eissn=1522-1598&rft.volume=106&rft.issue=2&rft.spage=630&rft.epage=640&rft_id=info:doi/10.1152%2Fjn.00015.2010&rft_id=info%3Apmid%2F21562186&rft.externalDocID=PMC3154804
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0022-3077&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0022-3077&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0022-3077&client=summon