Loss of interneurons and disruption of perineuronal nets in the cerebral cortex following hypoxia-ischaemia in near-term fetal sheep.

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dc.contributor.author Fowke, Tania M en
dc.contributor.author Galinsky, Robert en
dc.contributor.author Davidson, Joanne en
dc.contributor.author Wassink, Guido en
dc.contributor.author Karunasinghe, Rashika N en
dc.contributor.author Prasad, Jaya D en
dc.contributor.author Bennet, Laura en
dc.contributor.author Gunn, Alistair en
dc.contributor.author Dean, Justin en
dc.date.accessioned 2019-06-14T03:04:03Z en
dc.date.issued 2018-12-06 en
dc.identifier.citation Scientific reports 8(1):17686 06 Dec 2018 en
dc.identifier.issn 2045-2322 en
dc.identifier.uri http://hdl.handle.net/2292/47089 en
dc.description.abstract Hypoxia-ischaemia (HI) in term infants is a common cause of brain injury and neurodevelopmental impairment. Development of gamma-aminobutyric acid (GABA)ergic circuitry in the cerebral cortex is a critical event in perinatal brain development. Perineuronal nets (PNNs) are specialised extracellular matrix structures that surround GABAergic interneurons, and are important for their function. Herein, we hypothesised that HI would reduce survival of cortical interneurons and disrupt PNNs in a near-term fetal sheep model of global cerebral ischaemia. Fetal sheep (0.85 gestation) received sham occlusion (n = 5) or 30 min of reversible cerebral ischaemia (HI group; n = 5), and were recovered for 7 days. Expression of interneurons (glutamate decarboxylase [GAD]+; parvalbumin [PV]+) and PNNs (Wisteria floribunda agglutinin, WFA) was assessed in the parasagittal cortex by immunohistochemistry. HI was associated with marked loss of both GAD+ and PV+ cortical interneurons (all layers of the parasagittal cortex and layer 6) and PNNs (layer 6). The expression and integrity of PNNs was also reduced on surviving GAD+ interneurons. There was a trend towards a linear correlation of the proportion of GAD+ neurons that were WFA+ with seizure burden (r2 = 0.76, p = 0.0534). Overall, these data indicate that HI may cause deficits in the cortical GABAergic system involving loss of interneurons and disruption of PNNs, which may contribute to the range of adverse neurological outcomes following perinatal brain injury. en
dc.format.medium Electronic en
dc.language eng en
dc.relation.ispartofseries Scientific reports 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/4.0/ en
dc.subject Cerebral Cortex en
dc.subject Nerve Net en
dc.subject Interneurons en
dc.subject Extracellular Matrix en
dc.subject Animals en
dc.subject Sheep en
dc.subject GABAergic Neurons en
dc.subject Hypoxia en
dc.title Loss of interneurons and disruption of perineuronal nets in the cerebral cortex following hypoxia-ischaemia in near-term fetal sheep. en
dc.type Journal Article en
dc.identifier.doi 10.1038/s41598-018-36083-y en
pubs.issue 1 en
pubs.begin-page 17686 en
pubs.volume 8 en
dc.rights.holder Copyright: The authors en
pubs.publication-status Published en
dc.rights.accessrights http://purl.org/eprint/accessRights/OpenAccess en
pubs.subtype Research Support, Non-U.S. Gov't en
pubs.subtype research-article en
pubs.subtype Journal Article en
pubs.elements-id 758467 en
pubs.org-id Medical and Health Sciences en
pubs.org-id Medical Sciences en
pubs.org-id Physiology Division en
dc.identifier.eissn 2045-2322 en
pubs.record-created-at-source-date 2018-12-08 en
pubs.dimensions-id 30523273 en


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