E-2001, a novel anti-ischemic agent

Glutamic acid which accumulates extracellularly during cerebral ischemia is proposed to cause neuronal cell damage by acting as an excitotoxin. Thus, we measured extracellular glutamate in vitro and in vivo conditions and evaluated the activity of E-2001 , 2-「4-(p-fluorobenzoyl ) -piperidin-1-yl J-2...

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Bibliographic Details
Published inJapanese Journal of Pharmacology Vol. 46; no. suppl; p. 135
Main Authors Masuhiro Ikeda, Takahiro Nakazawa, Kouichi Abe, Takeru Kaneko, Kiyomi Yamatsu
Format Journal Article
LanguageJapanese
Published The Japanese Pharmacological Society 1988
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Summary:Glutamic acid which accumulates extracellularly during cerebral ischemia is proposed to cause neuronal cell damage by acting as an excitotoxin. Thus, we measured extracellular glutamate in vitro and in vivo conditions and evaluated the activity of E-2001 , 2-「4-(p-fluorobenzoyl ) -piperidin-1-yl J-2-acetonaphthone hydrochloride . Glutamate was analyzed by HPLC with spectrofluorometric detection. High potassiumevoked glutamate release from rat hippocampal slices was inhibited by E-2001 at concentrations of above 1×10^-6 M. Cerebral ischemia induced by 5-min occlusion of bilateral common carotid arteries in Mongolian gerbils caused marked increase in extracellular glutamate in hippocampus. Pretreatment of E-2001 (10 and 30 mg/kg, p.o.) completely protected the extracellular accumulation of glutamate. The inhibition of glutamate release by E-2001 may serve to ameliorate the ischemia-induced neuronal cell damage .
ISSN:0021-5198
1347-3506