Sexual dimorphism and brain lateralization impact behavioral and histological outcomes following hypoxia–ischemia in P3 and P7 rats

Sanches, Eduardo Farias; Arteni, Nice Sarmento; Nicola, Fabrício do Couto; Aristimunha, D.; Netto, Carlos Alexandre

doi:10.1016/j.neuroscience.2014.12.074

Cited by 50 publications

(42 citation statements)

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“…The Levine‐Rice model of HI is known to cause long term tissue damage and the most affected structure is the hippocampus ipsilateral to the carotid occlusion (Arteni et al, 2010; Sanches et al, 2015). Histological analysis performed at DPN45, 38 days after the injury, confirmed that the volumes of ipsilateral hippocampus and striatum were reduced in the lesioned groups; interestingly only the pre‐hypoxia treatment was able to protect against the HI insult.…”

Section: Discussionmentioning

confidence: 99%

Galantamine administration reduces reactive astrogliosis and upregulates the anti‐oxidant enzyme catalase in rats submitted to neonatal hypoxia ischemia

Odorcyk

Nicola

Durán‐Carabali

et al. 2017

Intl J of Devlp Neuroscience

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Neonatal hypoxia ischemia (HI) plays a role in the etiology of several neurological pathologies and causes severe sequelae. Acetylcholine is a neurotransmitter in the central nervous system and cholinesterase inhibitors have demonstrated a positive action over HI induced deficits. In order to evaluate the effects of pre and post-hypoxia administrations of galantamine, a cholinesterase inhibitor, in a model of perinatal HI, Wistar rats in the post-natal day 7 (PND7) were subjected to a combination of unilateral occlusion of the right carotid artery with the exposure to a 1h hypoxia. Intraperitoneal injections of galantamine were administered in two different protocols: one pre and other post-hypoxia. The analysis of brain structures volume at PND45 showed that pre-hypoxia galantamine treatment prevented tissue injury to the ipsilesional hippocampus. Also, immunofluorescence showed HI-induced increase in the number of astrocytes that was prevented by pre-hypoxia treatment. Biochemical analysis was performed in the ipsilesional hippocampus at PND8 and revealed that pre-hypoxia galantamine treatment: 1) prevented the neuronal loss induced by HI; 2) reduced the HI-induced hypertrophy of astrocytes; and 3) caused an increase in the activity of the anti-oxidant enzyme catalase. Overall, treatment with galantamine was able to prevent the brain damage, increase the survival of neurons, reduce astrocytic reaction and increase the activity of the anti-oxidant enzyme catalase in rats submitted to neonatal hypoxia ischemia.

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Section: Discussionmentioning

confidence: 99%

Galantamine administration reduces reactive astrogliosis and upregulates the anti‐oxidant enzyme catalase in rats submitted to neonatal hypoxia ischemia

Odorcyk

Nicola

Durán‐Carabali

et al. 2017

Intl J of Devlp Neuroscience

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“…Since neurotrophic signals induced by hop/STI1:PrP C interaction in central neurons depend on α7nAChR (Beraldo et al, 2010), and the latter has been implicated in neuronal resistance induced by either nicotine or melatonin against hypoxia (Hejmadi et al, 2003; Parada et al, 2014), the hop/STI1:PrP C :α7nAChR signaling complex may be a major player in neuroprotection against ischemic insults. Interestingly, examples of sexually dimorphic, ischemic brain injury mediated by both hormonal and non hormonal mechanisms (Liu et al, 2009; Herson and Hurn, 2010; Manwani and McCullough, 2011; Fairbanks et al, 2012; Herson et al, 2013; Zuo et al, 2013; Sanches et al, 2015) include the sensitivity of hippocampal neurons to ischemia in PrP C -null mice (Sakurai-Yamashita et al, 2005), and evidence has been reported of both sexually-dimorphic α-bungarotoxin binding (Arimatsu et al, 1981; Arimatsu and Seto, 1982) as well as changed content of α7nAChR following prenatal stress (Schulz et al, 2013). These data warrant a critical examination of the stoichiometry of hop/STI1:PrPC:α7nAChR complexes in the context of sensitivity to ischemic insults, especially in view of the variegated homo- and/or hetero-multimeric, cholinergic receptors that may assembled around α7nAChR subunits, as indicated by experimental work with various cell types (Bertrand et al, 2015; Wu et al, 2016).…”

Section: The Prion Protein As a Cell Surface Scaffold Proteinmentioning

confidence: 99%

The Biological Function of the Prion Protein: A Cell Surface Scaffold of Signaling Modules

Linden

2017

Front. Mol. Neurosci.

115

104

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The prion glycoprotein (PrPC) is mostly located at the cell surface, tethered to the plasma membrane through a glycosyl-phosphatydil inositol (GPI) anchor. Misfolding of PrPC is associated with the transmissible spongiform encephalopathies (TSEs), whereas its normal conformer serves as a receptor for oligomers of the β-amyloid peptide, which play a major role in the pathogenesis of Alzheimer’s Disease (AD). PrPC is highly expressed in both the nervous and immune systems, as well as in other organs, but its functions are controversial. Extensive experimental work disclosed multiple physiological roles of PrPC at the molecular, cellular and systemic levels, affecting the homeostasis of copper, neuroprotection, stem cell renewal and memory mechanisms, among others. Often each such process has been heralded as the bona fide function of PrPC, despite restricted attention paid to a selected phenotypic trait, associated with either modulation of gene expression or to the engagement of PrPC with a single ligand. In contrast, the GPI-anchored prion protein was shown to bind several extracellular and transmembrane ligands, which are required to endow that protein with the ability to play various roles in transmembrane signal transduction. In addition, differing sets of those ligands are available in cell type- and context-dependent scenarios. To account for such properties, we proposed that PrPC serves as a dynamic platform for the assembly of signaling modules at the cell surface, with widespread consequences for both physiology and behavior. The current review advances the hypothesis that the biological function of the prion protein is that of a cell surface scaffold protein, based on the striking similarities of its functional properties with those of scaffold proteins involved in the organization of intracellular signal transduction pathways. Those properties are: the ability to recruit spatially restricted sets of binding molecules involved in specific signaling; mediation of the crosstalk of signaling pathways; reciprocal allosteric regulation with binding partners; compartmentalized responses; dependence of signaling properties upon posttranslational modification; and stoichiometric requirements and/or oligomerization-dependent impact on signaling. The scaffold concept may contribute to novel approaches to the development of effective treatments to hitherto incurable neurodegenerative diseases, through informed modulation of prion protein-ligand interactions.

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“…The Rice‐Vannucci experimental model is commonly used to mimic HI insult observed in humans (Van De Looij et al, 2011). This model has provided information on the susceptibility of encephalic structures, such as cortex, striatum and hippocampus according to the brain maturation and impacts directly on sensorimotor and cognitive dysfunction (Durán‐Carabali et al, 2017; Sanches et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

Arundic acid administration protects astrocytes, recovers histological damage and memory deficits induced by neonatal hypoxia ischemia in rats

Mari

Odorcyk

Sanches³

et al. 2019

Intl J of Devlp Neuroscience

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Introduction Perinatal hypoxia‐ischemia (HI) is one of the main causes of mortality and chronic neurological morbidity in infants and children. Astrocytes play a key role in HI progression, becoming reactive in response to the injury, releasing S100 calcium binding protein B (S100B). Since S100B inhibition seems to have neuroprotective effects on central nervous system injury models, here we evaluated the neuroprotective effects of an S100B inhibitor, arundic acid (AA) in a HI model. Methods On the 7th postnatal day, animals were submitted to the combination of common carotid artery occlusion and hypoxic atmosphere (8% O2) for 60 min. Three experiments were performed in order to: (1) define AA dose (0.1, 1 or 10 mg/kg, pre‐hypoxia i.p. injection), (2) test if repeated AA administrations (10 mg/kg at 3 time points: Pre‐hypoxia, 24 h and 48 h after HI) would improve the response and (3) investigate biochemical mechanisms involved in AA protection two days after HI. Results AA at a dose of 10 mg/kg applied before and after hypoxia, was the only treatment protocol that was able to improve HI‐induced memory deficits, to reduce tissue damage, to promote astrocytic survival in the hippocampus and to reduced extracellular release of S100B in the cerebrospinal fluid. Conclusion Overall, AA treatment showed beneficial effects on memory deficits, tissue damage, promoting astrocyte survival likely by reducing S100B release. Protection aided to astrocytes by AA treatment against HI lesion may lead to development of new therapeutic strategies that target these particular cells.

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Sexual dimorphism and brain lateralization impact behavioral and histological outcomes following hypoxia–ischemia in P3 and P7 rats

Cited by 50 publications

References 98 publications

Galantamine administration reduces reactive astrogliosis and upregulates the anti‐oxidant enzyme catalase in rats submitted to neonatal hypoxia ischemia

Galantamine administration reduces reactive astrogliosis and upregulates the anti‐oxidant enzyme catalase in rats submitted to neonatal hypoxia ischemia

The Biological Function of the Prion Protein: A Cell Surface Scaffold of Signaling Modules

Arundic acid administration protects astrocytes, recovers histological damage and memory deficits induced by neonatal hypoxia ischemia in rats

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