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Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
Published on: November 20, 2015
Life-long effects of perinatal asphyxia on stress-induced proteins and dynamin 1 in rat brain
Erwin Kitzmueller1, Kurt Krapfenbauer, Harald Hoeger
1Department of Pediatrics, University of Vienna, Vienna, Austria.
Insights
Perinatal asphyxia (PA) in rats causes long-term changes in hippocampal protein expression, including increased stress proteins and decreased dynamin-1. These alterations may impact cognitive function and neuronal transport in aged rats.
Area of Science:
- Neuroscience
- Biochemistry
- Animal Models
Background:
- Perinatal asphyxia (PA) is known to cause lifelong cognitive and behavioral impairments.
- Previous research established PA's long-term effects on neurotransmitter deficits.
Purpose of the Study:
- To investigate long-term protein expression changes in the hippocampus of rats subjected to perinatal asphyxia.
- To identify specific proteins affected by PA at the end of the lifespan.
Main Methods:
- Utilized a validated rat model of perinatal asphyxia (20 min).
- Analyzed hippocampal tissue from 24-month-old normoxic and asphyxiated rats.
- Employed two-dimensional gel electrophoresis, MALDI-TOF, and specialized software for protein identification and quantification.
Main Results:
- Significantly increased levels of stress proteins: protein disulfide isomerase A3 precursor and stress-induced phosphoprotein-1.
- Significantly reduced levels of microtubule-associated protein dynamin-1.
- These changes were observed in the hippocampus of aged rats with a history of PA.
Conclusions:
- Elevated stress proteins may indicate persistent PA effects or adaptive neuroprotection.
- Reduced dynamin-1 suggests long-term impact on the exocytotic system and neuronal transport.
- These protein alterations could underlie impaired neuronal function and vesicle trafficking in aged rats post-PA.
Abstract:
In previous work, we have shown that perinatal asphyxia (PA) in the rat leads to life-long neurotransmitter deficits and impairment of cognitive functions and behavior. This observation made us examine protein expression in hippocampus of rats with PA at the end of the life span. We applied a well-documented and characterized animal model of PA. Pups, normoxic and asphyxiated for 20 min, were brought up until the age of 24 months and then were sacrificed. Hippocampal tissue was dissected from the brains, and proteins were run on two-dimensional gel electrophoresis with in-gel digestion and subsequent identification of proteins by MALDI-TOF followed by quantification of protein spots by specific software. In hippocampus of rats with PA, the stress proteins protein disulfide isomerase A3 precursor and stress-induced phosphoprotein-1 were significantly increased, whereas the microtubule-associated protein dynamin-1 was significantly reduced. Increased stress protein levels may represent long-term effects of PA or, alternatively, could reflect conditioning of the stress protein machinery known to occur as a neuroprotective principle following hypoxic-ischemic conditions. Decreased dynamin-1 levels may be considered as a long-term effect on the exocytotic system possibly reflecting or leading to impaired neuronal transport and vesicle-trafficking in PA of the rat of advanced age.
