scholarly journals Altered Astrocyte–Neuronal Interactions After Hypoxia-Ischemia in the Neonatal Brain in Female and Male Rats

Stroke ◽  
2014 ◽  
Vol 45 (9) ◽  
pp. 2777-2785 ◽  
Author(s):  
Tora Sund Morken ◽  
Eva Brekke ◽  
Asta Håberg ◽  
Marius Widerøe ◽  
Ann-Mari Brubakk ◽  
...  
2007 ◽  
Vol 208 (2) ◽  
pp. 269-276 ◽  
Author(s):  
Joseph Nuñez ◽  
Zhengang Yang ◽  
Yuhui Jiang ◽  
Theresa Grandys ◽  
Ilana Mark ◽  
...  

2016 ◽  
Vol 95 (1-2) ◽  
pp. 409-421 ◽  
Author(s):  
Carlos Alexandre Netto ◽  
Eduardo Sanches ◽  
Felipe Kawa Odorcyk ◽  
Luz Elena Duran-Carabali ◽  
Simone Nardin Weis

2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Kathryn M. Buller ◽  
Julie A. Wixey ◽  
Hanna E. Reinebrant

Identifying which specific neuronal phenotypes are vulnerable to neonatal hypoxia-ischemia, where in the brain they are damaged, and the mechanisms that produce neuronal losses are critical to determine the anatomical substrates responsible for neurological impairments in hypoxic-ischemic brain-injured neonates. Here we describe our current work investigating how the serotonergic network in the brain is disrupted in a rodent model of preterm hypoxia-ischemia. One week after postnatal day 3 hypoxia-ischemia, losses of serotonergic raphé neurons, reductions in serotonin levels in the brain, and reduced serotonin transporter expression are evident. These changes can be prevented using two anti-inflammatory interventions; the postinsult administration of minocycline or ibuprofen. However, each drug has its own limitations and benefits for use in neonates to stem damage to the serotonergic network after hypoxia-ischemia. By understanding the fundamental mechanisms underpinning hypoxia-ischemia-induced serotonergic damage we will hopefully move closer to developing a successful clinical intervention to treat neonatal brain injury.


Neuroreport ◽  
2008 ◽  
Vol 19 (10) ◽  
pp. 997-1002 ◽  
Author(s):  
Sylvie Girard ◽  
Annie Larouche ◽  
Hazim Kadhim ◽  
Marek Rola-Pleszczynski ◽  
Fernand Gobeil ◽  
...  

2020 ◽  
Vol 132 (5) ◽  
pp. 1080-1090 ◽  
Author(s):  
Anthony G. Hudetz ◽  
Siveshigan Pillay ◽  
Shiyong Wang ◽  
Heonsoo Lee

Abstract Background Neurocognitive investigations suggest that conscious sensory perception depends on recurrent neuronal interactions among sensory, parietal, and frontal cortical regions, which are suppressed by general anesthetics. The purpose of this work was to investigate if local interactions in sensory cortex are also altered by anesthetics. The authors hypothesized that desflurane would reduce recurrent neuronal interactions in cortical layer–specific manner consistent with the anatomical disposition of feedforward and feedback pathways. Methods Single-unit neuronal activity was measured in freely moving adult male rats (268 units; 10 animals) using microelectrode arrays chronically implanted in primary and secondary visual cortex. Layer-specific directional interactions were estimated by mutual information and transfer entropy of multineuron spike patterns within and between cortical layers three and five. The effect of incrementally increasing and decreasing steady-state concentrations of desflurane (0 to 8% to 0%) was tested for statistically significant quadratic trend across the successive anesthetic states. Results Desflurane produced robust, state-dependent reduction (P = 0.001) of neuronal interactions between primary and secondary visual areas and between layers three and five, as indicated by mutual information (37 and 41% decrease at 8% desflurane from wakeful baseline at [mean ± SD] 0.52 ± 0.51 and 0.53 ± 0.51 a.u., respectively) and transfer entropy (77 and 78% decrease at 8% desflurane from wakeful baseline at 1.86 ± 1.56 a.u. and 1.87 ± 1.67 a.u., respectively). In addition, a preferential suppression of feedback between secondary and primary visual cortex was suggested by the reduction of directional index of transfer entropy overall (P = 0.001; 89% decrease at 8% desflurane from 0.11 ± 0.18 a.u. at baseline) and specifically, in layer five (P = 0.001; 108% decrease at 8% desflurane from 0.12 ± 0.19 a.u. at baseline). Conclusions Desflurane anesthesia reduces neuronal interactions in visual cortex with a preferential effect on feedback. The findings suggest that neuronal disconnection occurs locally, among hierarchical sensory regions, which may contribute to global functional disconnection underlying anesthetic-induced unconsciousness. Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New


2020 ◽  
Author(s):  
Axel Erik Andersson ◽  
Carina Mallard ◽  
Carl Joakim Ek

Abstract BackgroundNeonatal hypoxia-ischemia often leads to lifelong disabilities with limited treatments currently available. The brain vasculature is an important factor in many neonatal brain pathologies but there is a lack of diagnostic tools to evaluate the brain vascular health of neonates in a clinical setting. Measurement of blood-brain barrier tight-junction proteins have shown promise as biomarkers for brain injury in the adult. Here we tested the biomarker potential of tight-junctions in the context of neonatal brain injury.MethodsThe levels of TJ-proteins (occluding, claudin-5, and zonula occludens-1) in both blood plasma and cerebrospinal fluid (CSF) as well as blood-brain barrier function were measured in a clinically relevant hypoxia/ischemia model in neonatal rats.ResultsTemporally acute elevated levels of occludin and claudin-5 could be measured in blood and CSF after hypoxia/ischemia with males generally having higher levels than females. The levels of claudin-5 in CSF correlated with the severity of the brain injury at 24h post- hypoxia/ischemia. Simultaneously, we detected early increase in blood-brain barrier-permeability at 6 and 24h after hypoxia/ischemia.ConclusionsLevels of circulating claudin-5 and occludin are increased after hypoxic/ischemic brain injuries and blood-brain barrier-impairment and have promise as early biomarkers for cerebral vascular health and as a tool for risk assessment of neonatal brain injuries.


2020 ◽  
Vol 112 ◽  
pp. 104343 ◽  
Author(s):  
Qing Yang ◽  
Ming-Fu Wu ◽  
Li-Hua Zhu ◽  
Li-Xing Qiao ◽  
Rui-Bin Zhao ◽  
...  

2018 ◽  
Vol 497 (1) ◽  
pp. 285-291 ◽  
Author(s):  
Rui-bin Zhao ◽  
Li-hua Zhu ◽  
Jia-Ping Shu ◽  
Li-Xing Qiao ◽  
Zheng-Kun Xia

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