NDLI: Glial hemichannels and their involvement in aging and neurodegenerative diseases.

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Glial hemichannels and their involvement in aging and neurodegenerative diseases.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Orellana, Juan A. Von Bernhardi, Rommy Giaume, Christian Sáez, Juan C.
Description	Country affiliation: Chile Author Affiliation: Orellana JA ( Facultad de Medicina, Departamento de Neurología, Pontificia Universidad Católica de Chile, Santiago, Chile. jaorella@uc.cl)
Abstract	During the last two decades, it became increasingly evident that glial cells accomplish a more important role in brain function than previously thought. Glial cells express pannexins and connexins, which are member subunits of two protein families that form membrane channels termed hemichannels. These channels communicate intra- and extracellular compartments and allow the release of autocrine/paracrine signaling molecules [e.g., adenosine triphosphate (ATP), glutamate, nicotinamide adenine dinucleotide, and prostaglandin E2] to the extracellular milieu, as well as the uptake of small molecules (e.g., glucose). An increasing body of evidence has situated glial hemichannels as potential regulators of the beginning and maintenance of homeostatic imbalances observed in diverse brain diseases. Here, we review and discuss the current evidence about the possible role of glial hemichannels on neurodegenerative diseases. A subthreshold pathological threatening condition leads to microglial activation, which keeps active defense and restores the normal function of the central nervous system. However, if the stimulus is deleterious, microglial cells and the endothelium become overactivated, both releasing bioactive molecules (e.g., glutamate, cytokines, prostaglandins, and ATP), which increase the activity of glial hemichannels, reducing the astroglial neuroprotective functions, and further reducing neuronal viability. Because ATP and glutamate are released via glial hemichannels in neurodegenerative conditions, it is expected that they contribute to neurotoxicity. More importantly, toxic molecules released via glial hemichannels could increase the Ca2+ entry in neurons also via neuronal hemichannels, leading to neuronal death. Therefore, blockade of hemichannels expressed by glial cells and/or neurons during neuroinflammation might prevent neurodegeneration.
File Format	HTM / HTML
ISSN	09688080
e-ISSN	14609576
Journal	Reviews in the Neurosciences
Issue Number	2
Volume Number	23
Language	English
Publisher	Taylor & Francis
Publisher Date	2012-01-26
Publisher Place	Germany
Access Restriction	Subscribed
Subject Keyword	Discipline Reproductive Medicine Aging Metabolism Cannabinoids Connexin 43 Connexins Ion Channels Physiology Nerve Degeneration Nerve Tissue Proteins Neurodegenerative Diseases Adenosine Triphosphate Astrocytes Calcium Pharmacology Central Nervous System Antagonists & Inhibitors Dinoprostone Glucose Glutamic Acid Inflammation Interleukin-1beta Nad Pathology Neurons Oligodendroglia Signal Transduction Tumor Necrosis Factor-alpha Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Reproductive Medicine Obstetrics and Gynecology

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