A M Panaitescu1, S Isac2, B Pavel2, A S Ilie3, M Ceanga2,4, A Totan5, L Zagrean2, G Peltecu1, A M Zagrean2. 1. "Carol Davila" University of Medicine and Pharmacy - Filantropia Hospital, Dept. of Obstetrics and Gynecology, Bucharest, Romania. 2. "Carol Davila" University of Medicine and Pharmacy - Physiology and Neuroscience, Bucharest, Romania. 3. University of Oxford - Department of Pharmacology, Oxford, United Kingdom of Great Britain and Northern Ireland. 4. Jena University Hospital - "Hans Berger" Department of Neurology, Jena, Germany. 5. "Carol Davila" University of Medicine and Pharmacy - Biochemistry, Bucharest, Romania.
Abstract
CONTEXT: Foetal asphyxia, a frequent birth complication, detrimentally impacts the immature brain, resulting in neuronal damage, uncontrolled seizure activity and long-term neurological deficits. Oxytocin, a neurohormone mediating important materno-foetal interactions and parturition, has been previously suggested to modulate the immature brain's excitability, playing a neuroprotective role. Our aim was to investigate the effects of exogenous oxytocin administration on seizure burden and acute brain injury in a perinatal model of asphyxia in rats. ANIMALS AND METHODS: Asphyxia was modelled by exposing immature rats to a 90-minute episode of low oxygen (9% O2) and high CO2 (20% CO2). Control rats were kept in ambient room-air for the same time interval. In a third group of experiments, oxytocin (0.02 UI/g body weight) was nasally administered 30 minutes before the asphyxia episode. Seizure burden was assessed by the cumulative number of loss of righting reflex (LRR) over a two-hour postexposure period. Acute brain injury was assessed through hippocampal S-100 beta, a biomarker of cellular injury, 24-hours after exposure. RESULTS: Asphyxia increased both LRR and hippocampal S-100 beta protein compared to controls, and these effects were significantly reduced by oxytocin administration. CONCLUSION: Oxytocin treatment decreased both seizure burden and hippocampal injury, supporting a potential neuroprotective role for oxytocin in perinatal asphyxia.
CONTEXT: Foetal asphyxia, a frequent birth complication, detrimentally impacts the immature brain, resulting in neuronal damage, uncontrolled seizure activity and long-term neurological deficits. Oxytocin, a neurohormone mediating important materno-foetal interactions and parturition, has been previously suggested to modulate the immature brain's excitability, playing a neuroprotective role. Our aim was to investigate the effects of exogenous oxytocin administration on seizure burden and acute brain injury in a perinatal model of asphyxia in rats. ANIMALS AND METHODS: Asphyxia was modelled by exposing immature rats to a 90-minute episode of low oxygen (9% O2) and high CO2 (20% CO2). Control rats were kept in ambient room-air for the same time interval. In a third group of experiments, oxytocin (0.02 UI/g body weight) was nasally administered 30 minutes before the asphyxia episode. Seizure burden was assessed by the cumulative number of loss of righting reflex (LRR) over a two-hour postexposure period. Acute brain injury was assessed through hippocampal S-100 beta, a biomarker of cellular injury, 24-hours after exposure. RESULTS: Asphyxia increased both LRR and hippocampal S-100 beta protein compared to controls, and these effects were significantly reduced by oxytocin administration. CONCLUSION: Oxytocin treatment decreased both seizure burden and hippocampal injury, supporting a potential neuroprotective role for oxytocin in perinatal asphyxia.
Entities:
Keywords:
S100B; hippocampus; loss of righting reflex; oxytocin; perinatal asphyxia
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