Differences in Hippocampal Protein Expression at 3 Days, 3 Weeks, and 3 Months Following Induction of Perinatal Asphyxia in the Rat

Weitzdörfer, Rachel; Höger, Harald; Burda, Gudrun; Pollak, Arnold; Lubec, Gert

doi:10.1021/pr700835y

Cited by 15 publications

(18 citation statements)

References 84 publications

(156 reference statements)

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“…Concomitantly, the same functional groups have been reported as resulting from research projects dedicated to the translational alterations identified by differential protein profiling [39]. These extensive alterations in the central molecular pathways can be potentially implicated in the development of potential asphyxia-related chronic complications, such as several sorts of degenerative processes in organs and onset of pre/cancerous lesions in the affected organs as summarised in Fig.…”

Section: Expression Profiling By “Gene Hunting”- Technology Discoverementioning

confidence: 82%

Birth asphyxia as the major complication in newborns: moving towards improved individual outcomes by prediction, targeted prevention and tailored medical care

et al. 2011

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Perinatal Asphyxia—oxygen deficit at delivery—can lead to severe hypoxic ischaemic organ damage in newborns followed by a fatal outcome or severe life-long pathologies. The severe insults often cause neurodegenerative diseases, mental retardation and epilepsies. The mild insults lead to so-called “minimal brain-damage disorders” such as attention deficits and hyperactivity, but can also be associated with the development of schizophrenia and life-long functional psychotic syndromes. Asphyxia followed by re-oxygenation can potentially lead to development of several neurodegenerative pathologies, diabetes type 2 and cancer. The task of individual prediction, targeted prevention and personalised treatments before a manifestation of the life-long chronic pathologies usually developed by newborns with asphyxic deficits, should be given the extraordinary priority in neonatology and paediatrics. Socio-economical impacts of educational measures and advanced strategies in development of robust diagnostic approaches targeted at effected molecular pathways, biomarker-candidates and potential drug-targets for tailored treatments are reviewed in the paper.

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Section: Expression Profiling By “Gene Hunting”- Technology Discoverementioning

confidence: 82%

Birth asphyxia as the major complication in newborns: moving towards improved individual outcomes by prediction, targeted prevention and tailored medical care

et al. 2011

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“…Protein extracts prepared were subjected to 2-DE as described elsewhere and 800 lg of protein were applied (Weitzdorfer et al, 2008).…”

Section: Two-dimensional Gel Electrophoresismentioning

confidence: 99%

Hippocampal synapsin isoform levels are linked to spatial memory enhancement by SGS742

John¹,

Sunyer²,

Höger³

et al. 2009

Hippocampus

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Synapsins are essential proteins for synaptic plasticity and there is no information available for their role in cognitive enhancement (CE) of spatial memory formation. It was therefore the aim of the study to link individual synapsin proteins and their isoforms to spatial memory formation enhanced by SGS742 in the mouse. Extracted hippocampal proteins from a cognitive study treating OF1 mice with the cognitive enhancer SGS742 and tested in the Morris water maze, were run on two-dimensional gel electrophoresis. Subsequently, protein spots were unambiguously identified by qQ-TOF mass spectrometry. Quantification of proteins from four groups (NaCl-treated mice, SGS742-treated mice, SGS742-treated yoked controls, and NaCl-treated yoked controls) was carried out according to an in-gel stable isotope labeling method. A total of 17 protein spots representing synapsin isoforms were identified and quantified. Using quantification of individual synapsin isoforms showed that these can be clearly assigned to CE by the GABAB antagonist SGS742. Quantitative determination of individual synapsin isoform showed an increase in SGS742-treated mice (mean+/-SD) of ratios between light and heavy stable isotope labeled synapsin protein (SGS742 vs. controls: 2.19+/-0.41 for synapsin Ia, and 1.41+/-0.81 for synapsin IIa). Synapsins Ib and IIb were not linked to CE. The NaCl-treated controls and the use of yoked controls that were ruling out swimming- and stress-mediated changes of synapsins, unequivocally allow to propose a role for synapsins Ia and IIa in the mechanism of CE of spatial memory formation.

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“…The consumption of extra energy for the reestablishment of homeostasis might compete with the demands required for circuitries and synapsis consolidation [55]. Several studies using the Swedish experimental model have reported distinct alterations induced by PA such as thickening of both pre- [32] and postsynaptic densities [24–29, 50]; protein misfolding, aggregation, and ubiquitination [24–29]; interruption of postnatal neurogenesis [58]; reduction in neurite length and branching [59, 60]; myelination deficits [63]; and modifications in the levels of synapsin [52, 60] and neurotrophic factors [61]. Some researchers have suggested the existence of plastic changes in an attempt to counterbalance neuronal loss [29, 32, 52, 57].…”

Section: Discussionmentioning

confidence: 99%

“…An Austrian group was also interested in protein derangements during postnatal development following PA and attempted to identify differentially expressed proteins that might represent potential biomarkers and pharmacological targets [52]. They decided to study hippocampal proteins following their own report of postnatal changes during brain development [53].…”

Section: Effects Of Experimental Perinatal Asphyxia On Synaptic Ormentioning

confidence: 99%

“…Interestingly synapsin IIb levels were increased. Weitzdörfer et al interpreted this finding as a result of both altered neurotransmitter release and compensatory synaptogenesis following PA [52]. The Swedish experimental model was selected for this study for its suitability to evaluate morphology, metabolism, neurochemistry, and long-term effects of PA [54].…”

Section: Effects Of Experimental Perinatal Asphyxia On Synaptic Ormentioning

confidence: 99%

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Could Perinatal Asphyxia Induce a Synaptopathy? New Highlights from an Experimental Model

et al. 2017

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Birth asphyxia also termed perinatal asphyxia is an obstetric complication that strongly affects brain structure and function. Central nervous system is highly susceptible to oxidative damage caused by perinatal asphyxia while activation and maturity of the proper pathways are relevant to avoiding abnormal neural development. Perinatal asphyxia is associated with high morbimortality in term and preterm neonates. Although several studies have demonstrated a variety of biochemical and molecular pathways involved in perinatal asphyxia physiopathology, little is known about the synaptic alterations induced by perinatal asphyxia. Nearly 25% of the newborns who survive perinatal asphyxia develop neurological disorders such as cerebral palsy and certain neurodevelopmental and learning disabilities where synaptic connectivity disturbances may be involved. Accordingly, here we review and discuss the association of possible synaptic dysfunction with perinatal asphyxia on the basis of updated evidence from an experimental model.

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Differences in Hippocampal Protein Expression at 3 Days, 3 Weeks, and 3 Months Following Induction of Perinatal Asphyxia in the Rat

Cited by 15 publications

References 84 publications

Birth asphyxia as the major complication in newborns: moving towards improved individual outcomes by prediction, targeted prevention and tailored medical care

Birth asphyxia as the major complication in newborns: moving towards improved individual outcomes by prediction, targeted prevention and tailored medical care

Hippocampal synapsin isoform levels are linked to spatial memory enhancement by SGS742

Could Perinatal Asphyxia Induce a Synaptopathy? New Highlights from an Experimental Model

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