New Insights on Astrocyte Ion Channels: Critical for Homeostasis and Neuron-Glia Signaling

Initial biophysical studies on glial cells nearly 50 years ago identified these cells as being electrically silent. These first studies also demonstrated a large K(+) conductance, which led to the notion that glia may regulate extracellular K(+) levels homeostatically. This view has now gained criti...

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Published in:The Journal of neuroscience Vol. 35; no. 41; pp. 13827 - 13835
Main Authors: Olsen, Michelle L, Khakh, Baljit S, Skatchkov, Serguei N, Zhou, Min, Lee, C Justin, Rouach, Nathalie
Format: Journal Article
Language:English
Published: United States Society for Neuroscience 14-10-2015
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Abstract Initial biophysical studies on glial cells nearly 50 years ago identified these cells as being electrically silent. These first studies also demonstrated a large K(+) conductance, which led to the notion that glia may regulate extracellular K(+) levels homeostatically. This view has now gained critical support from the study of multiple disease models discussed herein. Dysfunction of a major astrocyte K(+) channel, Kir4.1, appears as an early pathological event underlying neuronal phenotypes in several neurodevelopmental and neurodegenerative diseases. An expanding list of other astrocyte ion channels, including the calcium-activated ion channel BEST-1, hemichannels, and two-pore domain K(+) channels, all contribute to astrocyte biology and CNS function and underpin new forms of crosstalk between neurons and glia. Once considered merely the glue that holds the brain together, it is now increasingly recognized that astrocytes contribute in several fundamental ways to neuronal function. Emerging new insights and future perspectives of this active research area are highlighted within. The critical role of astrocyte potassium channels in CNS homeostasis has been reemphasized by recent studies conducted in animal disease models. Emerging evidence also supports the signaling role mediated by astrocyte ion channels such as BEST1, hemichannels, and two-pore channels, which enable astrocytes to interact with neurons and regulate synaptic transmission and plasticity. This minisymposium highlights recent developments and future perspectives of these research areas.
AbstractList Initial biophysical studies on glial cells nearly 50 years ago identified these cells as being electrically silent. These first studies also demonstrated a large K(+) conductance, which led to the notion that glia may regulate extracellular K(+) levels homeostatically. This view has now gained critical support from the study of multiple disease models discussed herein. Dysfunction of a major astrocyte K(+) channel, Kir4.1, appears as an early pathological event underlying neuronal phenotypes in several neurodevelopmental and neurodegenerative diseases. An expanding list of other astrocyte ion channels, including the calcium-activated ion channel BEST-1, hemichannels, and two-pore domain K(+) channels, all contribute to astrocyte biology and CNS function and underpin new forms of crosstalk between neurons and glia. Once considered merely the glue that holds the brain together, it is now increasingly recognized that astrocytes contribute in several fundamental ways to neuronal function. Emerging new insights and future perspectives of this active research area are highlighted within. SIGNIFICANCE STATEMENTThe critical role of astrocyte potassium channels in CNS homeostasis has been reemphasized by recent studies conducted in animal disease models. Emerging evidence also supports the signaling role mediated by astrocyte ion channels such as BEST1, hemichannels, and two-pore channels, which enable astrocytes to interact with neurons and regulate synaptic transmission and plasticity. This minisymposium highlights recent developments and future perspectives of these research areas.
Initial biophysical studies on glial cells nearly 50 years ago identified these cells as being electrically silent These first studies also demonstrated a large K+ conductance, which led to the notion that glia may regulate extracellular K+ levels homeostatically. This view has now gained critical support from the study of multiple disease models discussed herein. Dysfunction of a major astrocyte K+ channel, Kir4.1, appears as an early pathological event underlying neuronal phenotypes in several neurodevelopmental and neurodegenerative diseases. An expanding list of other astrocyte ion channels, including the calcium-activated ion channel BEST-1, hemichannels, and two-pore domain K+ channels, all contribute to astrocyte biology and CNS function and underpin new forms of crosstalk between neurons and glia. Once considered merely the glue that holds the brain together, it is now increasingly recognized that astrocytes contribute in several fundamental ways to neuronal function. Emerging new insights and future perspectives of this active research area are highlighted within.
Initial biophysical studies on glial cells nearly 50 years ago identified these cells as being electrically silent. These first studies also demonstrated a large K(+) conductance, which led to the notion that glia may regulate extracellular K(+) levels homeostatically. This view has now gained critical support from the study of multiple disease models discussed herein. Dysfunction of a major astrocyte K(+) channel, Kir4.1, appears as an early pathological event underlying neuronal phenotypes in several neurodevelopmental and neurodegenerative diseases. An expanding list of other astrocyte ion channels, including the calcium-activated ion channel BEST-1, hemichannels, and two-pore domain K(+) channels, all contribute to astrocyte biology and CNS function and underpin new forms of crosstalk between neurons and glia. Once considered merely the glue that holds the brain together, it is now increasingly recognized that astrocytes contribute in several fundamental ways to neuronal function. Emerging new insights and future perspectives of this active research area are highlighted within. The critical role of astrocyte potassium channels in CNS homeostasis has been reemphasized by recent studies conducted in animal disease models. Emerging evidence also supports the signaling role mediated by astrocyte ion channels such as BEST1, hemichannels, and two-pore channels, which enable astrocytes to interact with neurons and regulate synaptic transmission and plasticity. This minisymposium highlights recent developments and future perspectives of these research areas.
Initial biophysical studies on glial cells nearly 50 years ago identified these cells as being electrically silent. These first studies also demonstrated a large K + conductance, which led to the notion that glia may regulate extracellular K + levels homeostatically. This view has now gained critical support from the study of multiple disease models discussed herein. Dysfunction of a major astrocyte K + channel, Kir4.1, appears as an early pathological event underlying neuronal phenotypes in several neurodevelopmental and neurodegenerative diseases. An expanding list of other astrocyte ion channels, including the calcium-activated ion channel BEST-1, hemichannels, and two-pore domain K + channels, all contribute to astrocyte biology and CNS function and underpin new forms of crosstalk between neurons and glia. Once considered merely the glue that holds the brain together, it is now increasingly recognized that astrocytes contribute in several fundamental ways to neuronal function. Emerging new insights and future perspectives of this active research area are highlighted within. SIGNIFICANCE STATEMENT The critical role of astrocyte potassium channels in CNS homeostasis has been reemphasized by recent studies conducted in animal disease models. Emerging evidence also supports the signaling role mediated by astrocyte ion channels such as BEST1, hemichannels, and two-pore channels, which enable astrocytes to interact with neurons and regulate synaptic transmission and plasticity. This minisymposium highlights recent developments and future perspectives of these research areas.
Author Lee, C Justin
Rouach, Nathalie
Khakh, Baljit S
Olsen, Michelle L
Zhou, Min
Skatchkov, Serguei N
Author_xml – sequence: 1
  givenname: Michelle L
  surname: Olsen
  fullname: Olsen, Michelle L
  email: zhou.787@osu.edu, molsen@uab.edu
  organization: Department of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, Alabama 35294, zhou.787@osu.edu molsen@uab.edu
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  givenname: Baljit S
  surname: Khakh
  fullname: Khakh, Baljit S
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  givenname: Serguei N
  orcidid: 0000-0002-5397-7953
  surname: Skatchkov
  fullname: Skatchkov, Serguei N
  organization: Department of Biochemistry and Physiology, Universidad Central Del Caribe, Bayamón, Puerto Rico PR 00956
– sequence: 4
  givenname: Min
  surname: Zhou
  fullname: Zhou, Min
  email: zhou.787@osu.edu, molsen@uab.edu
  organization: Department of Neuroscience, Ohio State University Wexner Medical Center, Columbus, Ohio 43210, zhou.787@osu.edu molsen@uab.edu
– sequence: 5
  givenname: C Justin
  surname: Lee
  fullname: Lee, C Justin
  organization: Center for Neuroscience and Functional Connectomics, Brain Science Institute, Korea Institute of Science and Technology, Seoul, Republic of Korea, and
– sequence: 6
  givenname: Nathalie
  surname: Rouach
  fullname: Rouach, Nathalie
  organization: Neuroglial Interactions in Cerebral Physiopathology, Center for Interdisciplinary Research in Biology, Collège de France, INSERM U1050, CNRS UMR 7241, Labex Memolife, PSL Research University, Paris, France
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Issue 41
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Snippet Initial biophysical studies on glial cells nearly 50 years ago identified these cells as being electrically silent. These first studies also demonstrated a...
Initial biophysical studies on glial cells nearly 50 years ago identified these cells as being electrically silent These first studies also demonstrated a...
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SubjectTerms Animals
Biophysics
Homeostasis
Humans
Ion Channels - physiology
Life Sciences
Nervous System Diseases - genetics
Nervous System Diseases - metabolism
Nervous System Diseases - physiopathology
Neuroglia - physiology
Neurons - physiology
Signal Transduction - physiology
Symposium and Mini-Symposium
Title New Insights on Astrocyte Ion Channels: Critical for Homeostasis and Neuron-Glia Signaling
URI https://www.ncbi.nlm.nih.gov/pubmed/26468182
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Volume 35
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