Activity-dependent regulation of HCN1 protein in cortical neurons

Takeshi Arimitsu; Mutsuo Nuriya; Kazushige Ikeda; Takao Takahashi; Masato Yasui

doi:10.1016/j.bbrc.2009.06.127

Activity-dependent regulation of HCN1 protein in cortical neurons

Takeshi Arimitsu, Mutsuo Nuriya, Kazushige Ikeda, Takao Takahashi, Masato Yasui

Research output: Contribution to journal › Article › peer-review

10 Citations (Scopus)

Abstract

Homeostasis of neuronal activity is crucial to neuronal physiology. In dendrites, hyperpolarization-activated cyclic nucleotide-gated channel (HCN) 1 is considered to play critical roles in this process. While electrophysiological studies have demonstrated the dynamic modulation of I_h current mediated by HCN1 proteins, little is known about the underlying molecular and cellular mechanisms. In this study, we utilized cortical cultured neurons and biochemical methods to identify molecular and cellular mechanisms that mediate the physiological regulation of HCN1 channel functions in cortical neurons. Pharmacological manipulations of neuronal activity resulted in changes in the expression level of HCN1. In addition, the surface expression of HCN1 was dynamically regulated by neuronal activity. Both of these changes led to functional modulations of HCN1 channels. Our study suggests that coordinated changes in protein expression and surface expression of HCN1 serve as the key regulatory mechanisms controlling the function of endogenous HCN1 protein in cortical neurons.

Original language	English
Pages (from-to)	87-91
Number of pages	5
Journal	Biochemical and Biophysical Research Communications
Volume	387
Issue number	1
DOIs	https://doi.org/10.1016/j.bbrc.2009.06.127
Publication status	Published - 2009 Sept 11

Keywords

Cortical neuron
Homeostatic plasticity
Neuronal activity
Surface expression
Voltage-gated ion channel

ASJC Scopus subject areas

Biophysics
Biochemistry
Molecular Biology
Cell Biology

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10.1016/j.bbrc.2009.06.127

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@article{420ebd142bf6418da75c0e98a25d251a,

title = "Activity-dependent regulation of HCN1 protein in cortical neurons",

abstract = "Homeostasis of neuronal activity is crucial to neuronal physiology. In dendrites, hyperpolarization-activated cyclic nucleotide-gated channel (HCN) 1 is considered to play critical roles in this process. While electrophysiological studies have demonstrated the dynamic modulation of Ih current mediated by HCN1 proteins, little is known about the underlying molecular and cellular mechanisms. In this study, we utilized cortical cultured neurons and biochemical methods to identify molecular and cellular mechanisms that mediate the physiological regulation of HCN1 channel functions in cortical neurons. Pharmacological manipulations of neuronal activity resulted in changes in the expression level of HCN1. In addition, the surface expression of HCN1 was dynamically regulated by neuronal activity. Both of these changes led to functional modulations of HCN1 channels. Our study suggests that coordinated changes in protein expression and surface expression of HCN1 serve as the key regulatory mechanisms controlling the function of endogenous HCN1 protein in cortical neurons.",

keywords = "Cortical neuron, Homeostatic plasticity, Neuronal activity, Surface expression, Voltage-gated ion channel",

author = "Takeshi Arimitsu and Mutsuo Nuriya and Kazushige Ikeda and Takao Takahashi and Masato Yasui",

note = "Funding Information: This work was supported by Grants-in-Aid from the Ministry of Education, Culture, Sports, Science, and Technology (MEXT) of Japan, Keio University Research Grants for Life Science and Medicine, The Ichiro Kanehara Foundation and Global COE Program “Center for Human Metabolomic Systems Biology” from MEXT, Japan. We would like to thank Manae Imamura for excellent technical help, Mitsuko Shiota for administrative work, and members of the laboratory for their comments. Funding Information: Materials. The reagents for the neuronal cultures were purchased from Invitrogen (Carlsbad, CA, USA); all other chemicals were purchased from Sigma–Aldrich (St. Louis, MO, USA) unless otherwise stated. The anti-HCN1 monoclonal antibody N70/28 was developed by and obtained from the University of California at Davis/NINDS/NIMH NeuroMab Facility, supported by NIH Grant U24NS050606 and maintained by the Section of Neurobiology, Physiology and Behavior, College of Biological Sciences, University of California, Davis, CA 95616. ",

year = "2009",

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doi = "10.1016/j.bbrc.2009.06.127",

language = "English",

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AU - Arimitsu, Takeshi

AU - Nuriya, Mutsuo

AU - Ikeda, Kazushige

AU - Takahashi, Takao

AU - Yasui, Masato

N1 - Funding Information: This work was supported by Grants-in-Aid from the Ministry of Education, Culture, Sports, Science, and Technology (MEXT) of Japan, Keio University Research Grants for Life Science and Medicine, The Ichiro Kanehara Foundation and Global COE Program “Center for Human Metabolomic Systems Biology” from MEXT, Japan. We would like to thank Manae Imamura for excellent technical help, Mitsuko Shiota for administrative work, and members of the laboratory for their comments. Funding Information: Materials. The reagents for the neuronal cultures were purchased from Invitrogen (Carlsbad, CA, USA); all other chemicals were purchased from Sigma–Aldrich (St. Louis, MO, USA) unless otherwise stated. The anti-HCN1 monoclonal antibody N70/28 was developed by and obtained from the University of California at Davis/NINDS/NIMH NeuroMab Facility, supported by NIH Grant U24NS050606 and maintained by the Section of Neurobiology, Physiology and Behavior, College of Biological Sciences, University of California, Davis, CA 95616.

PY - 2009/9/11

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N2 - Homeostasis of neuronal activity is crucial to neuronal physiology. In dendrites, hyperpolarization-activated cyclic nucleotide-gated channel (HCN) 1 is considered to play critical roles in this process. While electrophysiological studies have demonstrated the dynamic modulation of Ih current mediated by HCN1 proteins, little is known about the underlying molecular and cellular mechanisms. In this study, we utilized cortical cultured neurons and biochemical methods to identify molecular and cellular mechanisms that mediate the physiological regulation of HCN1 channel functions in cortical neurons. Pharmacological manipulations of neuronal activity resulted in changes in the expression level of HCN1. In addition, the surface expression of HCN1 was dynamically regulated by neuronal activity. Both of these changes led to functional modulations of HCN1 channels. Our study suggests that coordinated changes in protein expression and surface expression of HCN1 serve as the key regulatory mechanisms controlling the function of endogenous HCN1 protein in cortical neurons.

AB - Homeostasis of neuronal activity is crucial to neuronal physiology. In dendrites, hyperpolarization-activated cyclic nucleotide-gated channel (HCN) 1 is considered to play critical roles in this process. While electrophysiological studies have demonstrated the dynamic modulation of Ih current mediated by HCN1 proteins, little is known about the underlying molecular and cellular mechanisms. In this study, we utilized cortical cultured neurons and biochemical methods to identify molecular and cellular mechanisms that mediate the physiological regulation of HCN1 channel functions in cortical neurons. Pharmacological manipulations of neuronal activity resulted in changes in the expression level of HCN1. In addition, the surface expression of HCN1 was dynamically regulated by neuronal activity. Both of these changes led to functional modulations of HCN1 channels. Our study suggests that coordinated changes in protein expression and surface expression of HCN1 serve as the key regulatory mechanisms controlling the function of endogenous HCN1 protein in cortical neurons.

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Activity-dependent regulation of HCN1 protein in cortical neurons

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Keywords

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