title: New Insights on Astrocyte Ion Channels: Critical for Homeostasis and Neuron-Glia Signaling.
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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, Alabama 35294, zhou.787@osu.edu molsen@uab.edu.
authors.forename: Michelle L
authors.initials: ML
authors.lastname: Olsen
authors.affiliation: Department of Physiology and Neurobiology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California 90095.
authors.forename: Baljit S
authors.initials: BS
authors.lastname: Khakh
authors.affiliation: Department of Biochemistry and Physiology, Universidad Central Del Caribe, Bayamón, Puerto Rico PR 00956.
authors.forename: Serguei N
authors.identifier: http://orcid.org/0000-0002-5397-7953
authors.initials: SN
authors.lastname: Skatchkov
authors.affiliation: Department of Neuroscience, Ohio State University Wexner Medical Center, Columbus, Ohio 43210, zhou.787@osu.edu molsen@uab.edu.
authors.forename: Min
authors.initials: M
authors.lastname: Zhou
authors.affiliation: Center for Neuroscience and Functional Connectomics, Brain Science Institute, Korea Institute of Science and Technology, Seoul, Republic of Korea, and.
authors.forename: C Justin
authors.initials: CJ
authors.lastname: Lee
authors.affiliation: 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.
authors.forename: Nathalie
authors.initials: N
authors.lastname: Rouach
mesh_terms: D000818:Animals; D001703:Biophysics; D006706:Homeostasis; D006801:Humans; D007473:Ion Channels / Q000502:physiology*; D009422:Nervous System Diseases / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology; D009457:Neuroglia / Q000502:physiology*; D009474:Neurons / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology*
chemical_list: D007473:Ion Channels