Gap junctions and hemichannels composed of connexins: potential therapeutic targets for neurodegenerative diseases

Microglia are macrophage-like resident immune cells that contribute to the maintenance of homeostasis in the central nervous system (CNS). Abnormal activation of microglia can cause damage in the CNS, and accumulation of activated microglia is a characteristic pathological observation in neurologic...

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Published inFrontiers in cellular neuroscience Vol. 8; p. 189
Main Authors Takeuchi, Hideyuki, Suzumura, Akio
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Research Foundation 02.09.2014
Frontiers Media S.A
Subjects
Amino acids
Amyotrophic lateral sclerosis
Animal models
Antigens
Cell adhesion & migration
Cell surface
Central nervous system
Connexins
Cytokines
Epilepsy
gap junction
Gap junctions
Glutamate
Homeostasis
Hypotheses
Immunology
Inflammation
Kinases
Macrophages
Microglia
Minocycline
Morphology
Multiple sclerosis
Neurodegeneration
Neurodegenerative diseases
Neurogenesis
Neuroinflammation
Neuronal-glial interactions
Neuroscience
Neurotoxicity
Physiology
Stroke
Therapeutic applications
Trauma
Tumor necrosis factor-TNF
neuroinflammation
hemichannel
neurodegeneration
gap junction
microglia
connexin
glutamate
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Abstract Microglia are macrophage-like resident immune cells that contribute to the maintenance of homeostasis in the central nervous system (CNS). Abnormal activation of microglia can cause damage in the CNS, and accumulation of activated microglia is a characteristic pathological observation in neurologic conditions such as trauma, stroke, inflammation, epilepsy, and neurodegenerative diseases. Activated microglia secrete high levels of glutamate, which damages CNS cells and has been implicated as a major cause of neurodegeneration in these conditions. Glutamate-receptor blockers and microglia inhibitors (e.g., minocycline) have been examined as therapeutic candidates for several neurodegenerative diseases; however, these compounds exerted little therapeutic benefit because they either perturbed physiological glutamate signals or suppressed the actions of protective microglia. The ideal therapeutic approach would hamper the deleterious roles of activated microglia without diminishing their protective effects. We recently found that abnormally activated microglia secrete glutamate via gap-junction hemichannels on the cell surface. Moreover, administration of gap-junction inhibitors significantly suppressed excessive microglial glutamate release and improved disease symptoms in animal models of neurologic conditions such as stroke, multiple sclerosis, amyotrophic lateral sclerosis, and Alzheimer's disease. Recent evidence also suggests that neuronal and glial communication via gap junctions amplifies neuroinflammation and neurodegeneration. Elucidation of the precise pathologic roles of gap junctions and hemichannels may lead to a novel therapeutic strategies that can slow and halt the progression of neurodegenerative diseases.
AbstractList Microglia are macrophage-like resident immune cells that contribute to the maintenance of homeostasis in the central nervous system (CNS). Abnormal activation of microglia can cause damage in the CNS, and accumulation of activated microglia is a characteristic pathological observation in neurologic conditions such as trauma, stroke, inflammation, epilepsy, and neurodegenerative diseases. Activated microglia secrete high levels of glutamate, which damages CNS cells and has been implicated as a major cause of neurodegeneration in these conditions. Glutamate-receptor blockers and microglia inhibitors (e.g., minocycline) have been examined as therapeutic candidates for several neurodegenerative diseases; however, these compounds exerted little therapeutic benefit because they either perturbed physiological glutamate signals or suppressed the actions of protective microglia. The ideal therapeutic approach would hamper the deleterious roles of activated microglia without diminishing their protective effects. We recently found that abnormally activated microglia secrete glutamate via gap-junction hemichannels on the cell surface. Moreover, administration of gap-junction inhibitors significantly suppressed excessive microglial glutamate release and improved disease symptoms in animal models of neurologic conditions such as stroke, multiple sclerosis, amyotrophic lateral sclerosis, and Alzheimer's disease. Recent evidence also suggests that neuronal and glial communication via gap junctions amplifies neuroinflammation and neurodegeneration. Elucidation of the precise pathologic roles of gap junctions and hemichannels may lead to a novel therapeutic strategies that can slow and halt the progression of neurodegenerative diseases.Microglia are macrophage-like resident immune cells that contribute to the maintenance of homeostasis in the central nervous system (CNS). Abnormal activation of microglia can cause damage in the CNS, and accumulation of activated microglia is a characteristic pathological observation in neurologic conditions such as trauma, stroke, inflammation, epilepsy, and neurodegenerative diseases. Activated microglia secrete high levels of glutamate, which damages CNS cells and has been implicated as a major cause of neurodegeneration in these conditions. Glutamate-receptor blockers and microglia inhibitors (e.g., minocycline) have been examined as therapeutic candidates for several neurodegenerative diseases; however, these compounds exerted little therapeutic benefit because they either perturbed physiological glutamate signals or suppressed the actions of protective microglia. The ideal therapeutic approach would hamper the deleterious roles of activated microglia without diminishing their protective effects. We recently found that abnormally activated microglia secrete glutamate via gap-junction hemichannels on the cell surface. Moreover, administration of gap-junction inhibitors significantly suppressed excessive microglial glutamate release and improved disease symptoms in animal models of neurologic conditions such as stroke, multiple sclerosis, amyotrophic lateral sclerosis, and Alzheimer's disease. Recent evidence also suggests that neuronal and glial communication via gap junctions amplifies neuroinflammation and neurodegeneration. Elucidation of the precise pathologic roles of gap junctions and hemichannels may lead to a novel therapeutic strategies that can slow and halt the progression of neurodegenerative diseases.
Microglia are macrophage-like resident immune cells that contribute to the maintenance of homeostasis in the central nervous system (CNS). Abnormal activation of microglia can cause damage in the CNS, and accumulation of activated microglia is a characteristic pathological observation in neurologic conditions such as trauma, stroke, inflammation, epilepsy, and neurodegenerative diseases. Activated microglia secrete high levels of glutamate, which damages CNS cells and has been implicated as a major cause of neurodegeneration in these conditions. Glutamate-receptor blockers and microglia inhibitors (e.g., minocycline) have been examined as therapeutic candidates for several neurodegenerative diseases; however, these compounds exerted little therapeutic benefit because they either perturbed physiological glutamate signals or suppressed the actions of protective microglia. The ideal therapeutic approach would hamper the deleterious roles of activated microglia without diminishing their protective effects. We recently found that abnormally activated microglia secrete glutamate via gap-junction hemichannels on the cell surface. Moreover, administration of gap-junction inhibitors significantly suppressed excessive microglial glutamate release and improved disease symptoms in animal models of neurologic conditions such as stroke, multiple sclerosis, amyotrophic lateral sclerosis, and Alzheimer's disease. Recent evidence also suggests that neuronal and glial communication via gap junctions amplifies neuroinflammation and neurodegeneration. Elucidation of the precise pathologic roles of gap junctions and hemichannels may lead to a novel therapeutic strategies that can slow and halt the progression of neurodegenerative diseases.
Author Takeuchi, Hideyuki
Suzumura, Akio
AuthorAffiliation Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University Nagoya, Japan
AuthorAffiliation_xml – name: Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University Nagoya, Japan
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  givenname: Hideyuki
  surname: Takeuchi
  fullname: Takeuchi, Hideyuki
– sequence: 2
  givenname: Akio
  surname: Suzumura
  fullname: Suzumura, Akio
BackLink https://www.ncbi.nlm.nih.gov/pubmed/25228858$$D View this record in MEDLINE/PubMed
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Keywords neuroinflammation
hemichannel
neurodegeneration
gap junction
microglia
connexin
glutamate
Language English
License This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
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Edited by: Juan Andrés Orellana, Pontificia Universidad Católica de Chile, Chile
This article was submitted to the journal Frontiers in Cellular Neuroscience.
Reviewed by: Juan C. Saez, Universidad Catolica de Chile, Chile; Georg Zoidl, York University, Canada; Eliseo A. Eugenin, Public Health Research Institute, USA
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PublicationTitle Frontiers in cellular neuroscience
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Snippet Microglia are macrophage-like resident immune cells that contribute to the maintenance of homeostasis in the central nervous system (CNS). Abnormal activation...
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StartPage 189
SubjectTerms Amino acids
Amyotrophic lateral sclerosis
Animal models
Antigens
Cell adhesion & migration
Cell surface
Central nervous system
Connexins
Cytokines
Epilepsy
gap junction
Gap junctions
Glutamate
Homeostasis
Hypotheses
Immunology
Inflammation
Kinases
Macrophages
Microglia
Minocycline
Morphology
Multiple sclerosis
Neurodegeneration
Neurodegenerative diseases
Neurogenesis
Neuroinflammation
Neuronal-glial interactions
Neuroscience
Neurotoxicity
Physiology
Stroke
Therapeutic applications
Trauma
Tumor necrosis factor-TNF
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Title Gap junctions and hemichannels composed of connexins: potential therapeutic targets for neurodegenerative diseases
URI https://www.ncbi.nlm.nih.gov/pubmed/25228858
https://www.proquest.com/docview/2278056734
https://www.proquest.com/docview/1563061062
https://pubmed.ncbi.nlm.nih.gov/PMC4151093
https://doaj.org/article/104c5669826e4da3bde85fe48482d281
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