Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province

Guangzhou, China

Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province

Guangzhou, China
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Wang Y.,Guangzhou Medical College | Wang Y.,Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province | Zhan L.,Guangzhou Medical College | Zhan L.,Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province | And 9 more authors.
Neurochemical Research | Year: 2011

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% O2 and 95% N2) 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. © 2011 Springer Science+Business Media, LLC.


Zhan L.,Guangzhou Medical College | Zhan L.,Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province | Wang T.,Guangzhou Medical College | Wang T.,Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province | And 7 more authors.
Journal of Neurochemistry | Year: 2010

It is well established that pre-conditioning protects neuronal injury against ischemia. However, the molecular mechanisms underlying ischemic tolerance are not completely understood. The purpose of the present study was to investigate the role of Akt/forkhead transcription factor, class O (FoxO) pathway in hypoxic pre-conditioning (HPC) using a newly developed HPC to transient global cerebral ischemia (tGCI) model in adult rats. HPC for 30-120 min significantly reduced cell death in the CA1 subregion after 10 min of tGCI. HPC was effective only when applied 1-4 days before ischemia. The maximum protection was observed with 30 min of hypoxia and 1 day interval between hypoxia and ischemia. The phosphorylated Akt and FoxOs measured by western blot and immunohistochemistry were significantly increased after hypoxia-ischemia except for a transient decrease in the HPC group. Lateral ventricular infusion of LY294002 before HPC blocked the increase in phosphorylated Akt and FoxOs and increased neuronal damage in HPC animals. These results suggest that pre-exposure to hypoxia induces protection against tGCI in adult rats. Activation of Akt results in the inactivation of FoxOs which may mediate ischemic tolerance after HPC. © 2010 International Society for Neurochemistry.

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