Journal
INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE
Volume 45, Issue -, Pages 66-74Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.ijdevneu.2014.12.007
Keywords
Cerebral ischemia; Connexin 43; Pannexin; Hemichannel; Neuroprotection; Fetal sheep
Categories
Funding
- Health Research Council of New Zealand [HRC 12/613]
- Auckland Medical Research Foundation
- Lottery Health Board of New Zealand
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Perinatal ischemic brain injury can occur as a result of a global ischemic insult or focal ischemic stroke in the preterm or full-term neonate. One of the most striking features of HI injury is that, after initial recovery of cellular oxidative metabolism, there is a delayed, 'secondary' mitochondrial failure that spreads over time from the most severely damaged areas outwards, into previously undamaged regions. This secondary failure is accompanied by transient seizure activity and cytotoxic edema. The specific mechanisms of this spread are poorly understood, but it is at least partly associated with spreading waves of depression that can trigger cell death in neighboring uninjured tissues. Both Connexin and Pannexin hemichannels may mediate release of paracrine molecules that in turn propagate cell death messages by releasing intracellular mediators, such as ATP, NAD(+), or glutamate or by abnormally prolonged opening to allow cell edema. This review will discuss the controversy around the relative contribution of both Connexin and Pannexin hemichannels and mechanisms by which they may contribute to the spread of ischemic brain injury. (C) 2014 Elsevier Ltd. All rights reserved.
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