Effects of interleukin-1β on hippocampal glutamate and GABA releases associated with Ca²⁺-induced Ca²⁺ releasing systems

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• 作者：Gang Zhu ; Motohiro Okada ; Shukuko Yoshida ; Fumiaki Mori ; Shinya Ueno ; Koichi Wakabayashi and Sunao Kaneko
• 关键词：Interleukin-1β ; Ca²⁺-induced Ca²⁺ releasing system ; Glutamate ; GABA ; Febrile seizure
• 刊名：Epilepsy Research
• 出版年：2006
• 出版时间：October 2006
• 年：2006
• 卷：71
• 期：2-3
• 页码：107-116
• 全文大小：431 K

文摘

Recent clinical and basic studies have demonstrated that hyperactivation of interleukin-1β (IL-1β) plays important roles in generation of febrile and epileptic seizures. To clarify this mechanism, the present study determined the effects of IL-1β on Ca²⁺-associated releases of glutamate and GABA in mouse hippocampus. Both basal and K⁺-evoked GABA releases were regulated by Ca²⁺ influx and Ca²⁺-induced Ca²⁺ releasing system (CICR). The K⁺-evoked glutamate release was also regulated by Ca²⁺ influx and CICR, whereas basal glutamate release was not affected by them. IL-1β increased basal releases of glutamate and GABA depending on the activation of Ca²⁺ influx and ryanodine receptor (RyR)-sensitive CICR, but reduced K⁺-evoked releases depending on Ca²⁺ influx, RyR-sensitive and inositol 1,4,5-trisphosphate receptor (IP3R)-sensitive CICRs. During neuronal hyperexcitability, the effect of IL-1β on GABA release was more predominantly modulated by Ca²⁺ influx and RyR-sensitive CICR than that on glutamate. These results indicate that hyperactivation of IL-1β leads to imbalance between glutamatergic and GABAergic transmission via toxic overload response of Ca²⁺ influx and CICR.