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KMID : 0811720050090000058
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Korean Journal of Physiology & Pharmacology
2005 Volume.9 No. 0 p.58 ~ p.0
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Simulated Ischemia Potentiation of GABAergic Neurotransmission in Mechanically Isolated Rat Cerebral Cortical Neurons
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Hahm Eu-Teum
Cho Kyung-Sook
Hwang Soon-Kyu
Lee Jong-Ju
Cho Young-Wuk
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Abstract
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Much interest of the neuronal death has focused on the release of glutamate during energy deprivation because of its excitotoxic actions. However, GABA release in ischemia is also to be important, because the activation of GABAA receptors will reduce the neuronal depolarization. The voltage change generated by spontaneous postsynaptic currents will contribute to the alteration of brain information processing that occurs early in ischemia. The oxygen-glucose deprivation (OGD) is a good in vitro model to study brain injury caused by ischemia/reperfusion. Reactive oxygen species (ROS) are generated during ischemia prior to reperfusion and participate in ischemia/reperfusion injury. Enhanced ROS production induces oxidative stress. Synaptic transmission of various neurotransmitters has been suggested to be sensitive to ROS. Hypoxia and hypoglycemia were also suggested to alter the GABA level. The present study was designed to investigate the modulatory effect of ROS, hypoxia, glucose-deprivation (GD) and OGD on GABAergic miniature inhibitory postsynaptic currents (mIPSCs) in cerebral cortical neurons. The cortical neurons with synaptic boutons were mechanically isolated from Sprague-Dawley rats (15~20 day-old). Hydrogen peroxide (HP, 1 mM) time-dependently and irreversibly increased the frequency and the current amplitude of GABAergic mIPSC. In the presence of 300-μM N-acetylcystein or 1,000-unit catalase, the HP-induced increase of neurotransmitter release frequency was not altered. In addition, 0.1-μM H-89 or 10-μM forskolin did not alter the modulatory effect of HP. GD and OGD time-dependently increased the frequency of GABAergic mIPSC without altering the current amplitude. However, hypoxia did not alter the frequency or the amplitude of GABAergic mIPSCs. This work was supported by a grant No. R13-2002-020-01003-0 from the Korea Science & Engineering Foundation.
Source: Korean Journal of Physiology & Pharmacology.2005 Oct;9(Suppl I):S84-S84
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KEYWORD
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Ischemia, Hydrogen peroxide, GABA, Synaptic transmission, Cerebral cortex
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