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Glia and hemichannels: key mediators of perinatal encephalopathy

Authors :
Robert Galinsky
Joanne O Davidson
Justin M Dean
Colin R Green
Laura Bennet
Alistair J Gunn
Source :
Neural Regeneration Research, Vol 13, Iss 2, Pp 181-189 (2018)
Publication Year :
2018
Publisher :
Wolters Kluwer Medknow Publications, 2018.

Abstract

Perinatal encephalopathy remains a major cause of disability, such as cerebral palsy. Therapeutic hypothermia is now well established to partially reduce risk of disability in late preterm/term infants. However, new and complementary therapeutic targets are needed to further improve outcomes. There is increasing evidence that glia play a key role in neural damage after hypoxia-ischemia and infection/inflammation. In this review, we discuss the role of astrocytic gap junction (connexin) hemichannels in the spread of neural injury after hypoxia-ischemia and/or infection/inflammation. Potential mechanisms of hemichannel mediated injury likely involve impaired intracellular calcium handling, loss of blood-brain barrier integrity and release of adenosine triphosphate (ATP) resulting in over-activation of purinergic receptors. We propose the hypothesis that inflammation-induced opening of connexin hemichannels is a key regulating event that initiates a vicious cycle of excessive ATP release, which in turn propagates activation of purinergic receptors on microglia and astrocytes. This suggests that developing new neuroprotective strategies for preterm infants will benefit from a detailed understanding of glial and connexin hemichannel responses.

Details

Language :
English
ISSN :
16735374
Volume :
13
Issue :
2
Database :
Directory of Open Access Journals
Journal :
Neural Regeneration Research
Publication Type :
Academic Journal
Accession number :
edsdoj.b60622fb42b948f19251ec3035272529
Document Type :
article
Full Text :
https://doi.org/10.4103/1673-5374.226378