HCN1 subunits contribute to the kinetics of I(h) in neonatal cortical plate neurons

Luminita Stoenica; Wiebke Wilkars; Arne Battefeld; Konstantin Stadler; Roland Bender; Ulf Strauss

doi:10.1002/dneu.22104

HCN1 subunits contribute to the kinetics of I(h) in neonatal cortical plate neurons

Standard

HCN1 subunits contribute to the kinetics of I(h) in neonatal cortical plate neurons. / Stoenica, Luminita; Wilkars, Wiebke; Battefeld, Arne; Stadler, Konstantin; Bender, Roland; Strauss, Ulf.

In: Developmental neurobiology, Vol. 73, No. 10, 01.10.2013, p. 785-97.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Stoenica, L, Wilkars, W, Battefeld, A, Stadler, K, Bender, R & Strauss, U 2013, 'HCN1 subunits contribute to the kinetics of I(h) in neonatal cortical plate neurons', Developmental neurobiology, vol. 73, no. 10, pp. 785-97. https://doi.org/10.1002/dneu.22104

APA

Stoenica, L., Wilkars, W., Battefeld, A., Stadler, K., Bender, R., & Strauss, U. (2013). HCN1 subunits contribute to the kinetics of I(h) in neonatal cortical plate neurons. Developmental neurobiology, 73(10), 785-97. https://doi.org/10.1002/dneu.22104

Vancouver

Stoenica L, Wilkars W, Battefeld A, Stadler K, Bender R, Strauss U. HCN1 subunits contribute to the kinetics of I(h) in neonatal cortical plate neurons. Developmental neurobiology. 2013 Oct 1;73(10):785-97. https://doi.org/10.1002/dneu.22104

Bibtex

@article{1916f0ddf15a4a58ab45389761fcc94b,

title = "HCN1 subunits contribute to the kinetics of I(h) in neonatal cortical plate neurons",

abstract = "The distribution of ion channels in neurons regulates neuronal activity and proper formation of neuronal networks during neuronal development. One of the channels is the hyperpolarization-activated cyclic nucleotide-gated (HCN) channel constituting the molecular substrate of hyperpolarization-activated current (I(h)). Our previous study implied a role for the fastest activating subunit HCN1 in the generation of Ih in rat neonatal cortical plate neurons. To better understand the impact of HCN1 in early neocortical development, we here performed biochemical analysis and whole-cell recordings in neonatal cortical plate and juvenile layer 5 somatosensory neurons of HCN1(-/-) and control HCN1(+/+) mice. Western Blot analysis revealed that HCN1 protein expression in neonatal cortical plate tissue of HCN(+/+) mice amounted to only 3% of the HCN1 in young adult cortex and suggested that in HCN1(-/-) mice other isoforms (particularly HCN4) might be compensatory up-regulated. At the first day after birth, functional ablation of the HCN1 subunit did not affect the proportion of Ih expressing pyramidal cortical plate neurons. Although the contribution of individual subunit proteins remains open, the lack of HCN1 markedly slowed the current activation and deactivation in individual I(h) expressing neurons. However, it did not impair maximal amplitude/density, voltage dependence of activation, and cAMP sensitivity. In conclusion, our data imply that, although expression is relatively low, HCN1 contributes substantially to I(h) properties in individual cortical plate neurons. These properties are significantly changed in HCN1(-/-), either due to the lack of HCN1 itself or due to compensatory mechanisms.",

keywords = "Animals, Animals, Newborn, Cyclic Nucleotide-Gated Cation Channels, Female, Gene Knockout Techniques, Hippocampus, Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels, Kinetics, Membrane Potentials, Mice, Mice, 129 Strain, Neurons, Potassium Channels, Pyramidal Cells, Rats, Rats, Wistar",

author = "Luminita Stoenica and Wiebke Wilkars and Arne Battefeld and Konstantin Stadler and Roland Bender and Ulf Strauss",

note = "Copyright {\textcopyright} 2013 Wiley Periodicals, Inc.",

year = "2013",

month = oct,

day = "1",

doi = "10.1002/dneu.22104",

language = "English",

volume = "73",

pages = "785--97",

journal = "DEV NEUROBIOL",

issn = "1932-8451",

publisher = "John Wiley and Sons Inc.",

number = "10",

}

RIS

TY - JOUR

T1 - HCN1 subunits contribute to the kinetics of I(h) in neonatal cortical plate neurons

AU - Stoenica, Luminita

AU - Wilkars, Wiebke

AU - Battefeld, Arne

AU - Stadler, Konstantin

AU - Bender, Roland

AU - Strauss, Ulf

PY - 2013/10/1

Y1 - 2013/10/1

N2 - The distribution of ion channels in neurons regulates neuronal activity and proper formation of neuronal networks during neuronal development. One of the channels is the hyperpolarization-activated cyclic nucleotide-gated (HCN) channel constituting the molecular substrate of hyperpolarization-activated current (I(h)). Our previous study implied a role for the fastest activating subunit HCN1 in the generation of Ih in rat neonatal cortical plate neurons. To better understand the impact of HCN1 in early neocortical development, we here performed biochemical analysis and whole-cell recordings in neonatal cortical plate and juvenile layer 5 somatosensory neurons of HCN1(-/-) and control HCN1(+/+) mice. Western Blot analysis revealed that HCN1 protein expression in neonatal cortical plate tissue of HCN(+/+) mice amounted to only 3% of the HCN1 in young adult cortex and suggested that in HCN1(-/-) mice other isoforms (particularly HCN4) might be compensatory up-regulated. At the first day after birth, functional ablation of the HCN1 subunit did not affect the proportion of Ih expressing pyramidal cortical plate neurons. Although the contribution of individual subunit proteins remains open, the lack of HCN1 markedly slowed the current activation and deactivation in individual I(h) expressing neurons. However, it did not impair maximal amplitude/density, voltage dependence of activation, and cAMP sensitivity. In conclusion, our data imply that, although expression is relatively low, HCN1 contributes substantially to I(h) properties in individual cortical plate neurons. These properties are significantly changed in HCN1(-/-), either due to the lack of HCN1 itself or due to compensatory mechanisms.

AB - The distribution of ion channels in neurons regulates neuronal activity and proper formation of neuronal networks during neuronal development. One of the channels is the hyperpolarization-activated cyclic nucleotide-gated (HCN) channel constituting the molecular substrate of hyperpolarization-activated current (I(h)). Our previous study implied a role for the fastest activating subunit HCN1 in the generation of Ih in rat neonatal cortical plate neurons. To better understand the impact of HCN1 in early neocortical development, we here performed biochemical analysis and whole-cell recordings in neonatal cortical plate and juvenile layer 5 somatosensory neurons of HCN1(-/-) and control HCN1(+/+) mice. Western Blot analysis revealed that HCN1 protein expression in neonatal cortical plate tissue of HCN(+/+) mice amounted to only 3% of the HCN1 in young adult cortex and suggested that in HCN1(-/-) mice other isoforms (particularly HCN4) might be compensatory up-regulated. At the first day after birth, functional ablation of the HCN1 subunit did not affect the proportion of Ih expressing pyramidal cortical plate neurons. Although the contribution of individual subunit proteins remains open, the lack of HCN1 markedly slowed the current activation and deactivation in individual I(h) expressing neurons. However, it did not impair maximal amplitude/density, voltage dependence of activation, and cAMP sensitivity. In conclusion, our data imply that, although expression is relatively low, HCN1 contributes substantially to I(h) properties in individual cortical plate neurons. These properties are significantly changed in HCN1(-/-), either due to the lack of HCN1 itself or due to compensatory mechanisms.

KW - Animals

KW - Animals, Newborn

KW - Cyclic Nucleotide-Gated Cation Channels

KW - Female

KW - Gene Knockout Techniques

KW - Hippocampus

KW - Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels

KW - Kinetics

KW - Membrane Potentials

KW - Mice

KW - Mice, 129 Strain

KW - Neurons

KW - Potassium Channels

KW - Pyramidal Cells

KW - Rats

KW - Rats, Wistar

U2 - 10.1002/dneu.22104

DO - 10.1002/dneu.22104

M3 - SCORING: Journal article

C2 - 23821600

VL - 73

SP - 785

EP - 797

JO - DEV NEUROBIOL

JF - DEV NEUROBIOL

SN - 1932-8451

IS - 10

ER -