Glia and hemichannels: key mediators of perinatal encephalopathy.

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dc.contributor.author Galinsky, Robert en
dc.contributor.author Davidson, Joanne en
dc.contributor.author Dean, Justin en
dc.contributor.author Green, Colin en
dc.contributor.author Bennet, Laura en
dc.contributor.author Gunn, Alistair en
dc.date.accessioned 2018-12-02T22:28:21Z en
dc.date.issued 2018-02 en
dc.identifier.citation Neural regeneration research 13(2):181-189 Feb 2018 en
dc.identifier.issn 1673-5374 en
dc.identifier.uri http://hdl.handle.net/2292/44745 en
dc.description.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. en
dc.format.medium Print en
dc.language eng en
dc.relation.ispartofseries Neural regeneration research en
dc.rights Items in ResearchSpace are protected by copyright, with all rights reserved, unless otherwise indicated. Previously published items are made available in accordance with the copyright policy of the publisher. en
dc.rights.uri https://researchspace.auckland.ac.nz/docs/uoa-docs/rights.htm en
dc.rights.uri https://creativecommons.org/licenses/by-sa/4.0/ en
dc.title Glia and hemichannels: key mediators of perinatal encephalopathy. en
dc.type Journal Article en
dc.identifier.doi 10.4103/1673-5374.226378 en
pubs.issue 2 en
pubs.begin-page 181 en
pubs.volume 13 en
dc.rights.holder Copyright: The author en
dc.identifier.pmid 29557357 en
pubs.end-page 189 en
pubs.publication-status Published en
dc.rights.accessrights http://purl.org/eprint/accessRights/OpenAccess en
pubs.subtype review-article en
pubs.subtype Review en
pubs.subtype Journal Article en
pubs.elements-id 732851 en
pubs.org-id Medical and Health Sciences en
pubs.org-id Medical Sciences en
pubs.org-id Physiology Division en
pubs.org-id Science en
pubs.org-id Science Research en
pubs.org-id Maurice Wilkins Centre (2010-2014) en
dc.identifier.eissn 1876-7958 en
pubs.record-created-at-source-date 2018-03-21 en
pubs.dimensions-id 29557357 en


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