Hypoxic Response of Synaptosomal Proteins in Term Guinea Pig Fetuses

doi:10.1046/j.1471-4159.1999.02139.x

Cited by 30 publications

(1 citation statement)

References 45 publications

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“…Synaptosomal purification from cortical neurons was performed by using a well-established method described by Booth and Clark (1978) , Razdan et al (1993), and Buonocore et al (1999) . In brief, cortical tissue was homogenized in an isolation medium (0.32 M sucrose/l mM potassium EDTA/lOmM Tris-HCl, pH7.4), followed by centrifugation to isolate a mitochondrial/synaptosomal pellet.…”

Section: Methodsmentioning

confidence: 99%

Hypercapnia Causes Injury of the Cerebral Cortex and Cognitive Deficits in Newborn Piglets

Fritz,

Sanidas,

Cardenas

et al. 2024

eNeuro

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In critically ill newborns, exposure to hypercapnia (HC) is common and often accepted in neonatal intensive care units (NICUs) to prevent severe lung injury. However, as a “safe” range of arterial partial pressure of carbon dioxide (PaCO2) levels in neonates has not been established, the potential impact of HC on the neurodevelopmental outcomes in these newborns remains a matter of concern. Here, in a newborn Yorkshire piglet model of either sex, we show that acute exposure to HC induced persistent cortical neuronal injury, associated cognitive and learning deficits, and long-term suppression of cortical electroencephalographic (EEG) frequencies. HC induced a transient energy failure in cortical neurons, a persistent dysregulation of calcium-dependent pro-apoptotic signaling in the cerebral cortex, and activation of the apoptotic cascade, leading to nuclear deoxyribonucleic acid (DNA) fragmentation. While neither one hour of HC nor the rapid normalization of HC were associated with changes in cortical bioenergetics, rapid resuscitation resulted in a delayed onset of synaptosomal membrane lipid peroxidation, suggesting a dissociation between energy failure and the occurrence of synaptosomal lipid peroxidation. Even short durations of HC triggered biochemical responses at the subcellular level of the cortical neurons resulting in altered cortical activity and impaired neurobehavior. The deleterious effects of HC on the developing brain should be carefully considered as crucial elements of clinical decisions in the neonatal intensive care unit.Significance StatementHospitalized critically ill neonates commonly experience hypercapnia as part of common practice in neonatal intensive care, as ventilated newborns are subjected to "permissive hypercapnia" to reduce lung injury associated with positive pressure ventilation. To answer the clinically important question of how "safe" that practice is, the present study provides new insights into the complex effects of hypercapnia on neuronal processes, with significant ramifications for ongoing neurodevelopment.

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Section: Methodsmentioning

confidence: 99%

Hypercapnia Causes Injury of the Cerebral Cortex and Cognitive Deficits in Newborn Piglets

Fritz,

Sanidas,

Cardenas

et al. 2024

eNeuro

View full text Add to dashboard Cite

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Neuroproteomics in neurotrauma

Ottens

Kobeissy

Golden

et al. 2006

Mass Spectrometry Reviews

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Neurotrauma in the form of traumatic brain injury (TBI) afflicts more Americans annually than Alzheimer's and Parkinson's disease combined, yet few researchers have used neuroproteomics to investigate the underlying complex molecular events that exacerbate TBI. Discussed in this review is the methodology needed to explore the neurotrauma proteome-from the types of samples used to the mass spectrometry identification and quantification techniques available. This neuroproteomics survey presents a framework for large-scale protein research in neurotrauma, as applied for immediate TBI biomarker discovery and the far-reaching systems biology understanding of how the brain responds to trauma. Ultimately, knowledge attained through neuroproteomics could lead to clinical diagnostics and therapeutics to lessen the burden of neurotrauma on society.

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Proteomic approach to the identification of voltage‐dependent anion channel protein isoforms in guinea pig brain synaptosomes

et al. 2004

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Voltage-dependent anion channel (VDAC) proteins are small, abundant, pore-forming proteins belonging to the eukaryotic mitochondrial porins. At least three different VDAC genes have been identified in vertebrates. VDAC proteins are known to play an essential role in cellular metabolism and in the early stages of apoptosis. A proteomic approach, consisting of two-dimensional gel electrophoresis followed by two-dimensional immunoblotting with anti-VDAC and anti-phosphotyrosine antibodies and by matrix-assisted laser desorption/ionization-time of flight mass spectrometry, was exploited to define the expression pattern of VDAC isoforms in guinea pig brain synaptosomes, both in normoxic and hypoxic conditions. In this way a total of five different VDAC isoforms were identified, as both VDAC1 and VDAC2 were detected in more than one electrophoretic spot. Moreover, VDAC isoforms selectively undergo hypoxia-induced tyrosine phosphorylation, suggesting that tyrosine phosphorylation may contribute to the modulation of VDAC protein function/conformation or interaction with other proteins in hypoxic conditions.

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Hypoxic Response of Synaptosomal Proteins in Term Guinea Pig Fetuses

Cited by 30 publications

References 45 publications

Hypercapnia Causes Injury of the Cerebral Cortex and Cognitive Deficits in Newborn Piglets

Hypercapnia Causes Injury of the Cerebral Cortex and Cognitive Deficits in Newborn Piglets

Neuroproteomics in neurotrauma

Proteomic approach to the identification of voltage‐dependent anion channel protein isoforms in guinea pig brain synaptosomes

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