Downregulation of Hippocampal GABA after Hypoxia-Induced Seizures in Neonatal Rats

This study aims to determine the expression of Gamma-aminobutyric acid (GABA) following hypoxia in neonatal rats and explore how it may increase susceptibility to epilepsy later in life. A modified model of neonatal hypoxia-induced epileptic susceptibility was simulated by 17 min of hypoxia (5% O 2...

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Bibliographic Details
Published in:Neurochemical research 2011-12, Vol.36 (12), p.2409-2416
Main Authors: Wang, Yanmei, Zhan, Lixuan, Zeng, Wei, Li, Ke, Sun, Weiwen, Xu, Zao C., Xu, En
Format: Article
Language:English
Subjects:
Animals
Animals, Newborn
Biochemistry
Biomedical and Life Sciences
Biomedicine
Cell Biology
Disease Susceptibility
Down-Regulation
Epilepsy - etiology
gamma-Aminobutyric Acid - biosynthesis
Glutamate Decarboxylase - biosynthesis
Hippocampus - metabolism
Hippocampus - pathology
Hypoxia - complications
Neurochemistry
Neurology
Neurosciences
Original Paper
Parvalbumins - metabolism
Rats
Rats, Sprague-Dawley
Seizures - metabolism
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Summary:This study aims to determine the expression of Gamma-aminobutyric acid (GABA) following hypoxia in neonatal rats and explore how it may increase susceptibility to epilepsy later in life. A modified model of neonatal hypoxia-induced epileptic susceptibility was simulated by 17 min of hypoxia (5% O 2 and 95% N 2 ) in postnatal day (P) 10 rats. Hippocampal glutamate decarboxylase (GAD) and parvalbumin (PV) during the development with or without hypoxia were examined using immunohistochemistry. No detectable neuronal loss was observed in the hippocampus either immediately or 14 days after hypoxia. During the development GAD- and PV-immunoreactivity increased substantially during P 11–13 and reached mature expression in the control rats, and decreased significantly at different time points except for a transient increase during P 11–13 in the hypoxic groups. Our study indicates that downregulation of hippocampal GABA after hypoxia-induced seizures in neonatal rats may contribute to higher epileptic susceptibility in later life.
ISSN:0364-3190
1573-6903
DOI:10.1007/s11064-011-0565-4