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Kainic Acid¿¡ ÀÇÇÑ ÈòÁã Çظ¶ÀÇ ¼Õ»ó°úÁ¤¿¡¼­ RPIA°¡ ¹ÌÄ¡´Â ¿µÇâ¿¡ °üÇÑ ÇüÅÂÇÐÀû ¿¬±¸ A Morphological Study on the Effects of RPIA on Kainic Acid-induced Neurotoxicity in the Hippocampus in Rats

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½Åµ¿Áø ( Shin Dong-Jin ) 
ÀÎõ Á߾ӱ溴¿ø ½Å°æ°ú

Ȳ¼¼Áø ( Hwang Se-Jin ) 
ÇѾç´ëÇб³ ÀÇ°ú´ëÇÐ ÇغÎ.¼¼Æ÷»ý¹°Çб³½Ç
Á¤È£»ï ( Chung Ho-Sam ) 
ÇѾç´ëÇб³ ÀÇ°ú´ëÇÐ ÇغÎÇб³½Ç

Abstract


Systemic injection of kainic acid (KA) in experimental animals induces the limbic seizure and structural damages in hippocampus and amygdala which resemble the changes in human temporal lobe epilepsy. In recent reports, some adenosine analogues exert neuroprotective actions against excitatory or ischemic neurotoxicity by several mechanisms. The author performed this study to investigate the neuroprotective effects of an adenosine agonist, R-phenylisopropyl adenosine (RPIA), on the neurotoxicity induced by KA in the hippocampus in rats. Kainic acid (10 §·/§¸) was administered intraperitoneally, and coadministration of KA with RPIA (100 §¶/§¸, i p. 10 min prior to injection of KA), wase also performed. The experimental animals were sacrificed at 1 day and 1 week after drug administration. Luxol frost blue cresyl violet stain and GFAP immunohistochemistry in hippocampus were performed. Loss of pyramidal cells in CA1 and CA3 of hippocampus and increase of GFAP immunoreactivity in the dentate gyrus and all hippocampal area were observed 1 day and 1 week after KA injection. Neuronal atrophy and nuclear pyknosis were observed but substantial cell loss was not found after coadministration of KA with RPIA. GFAP immunoreactivity in the hippocampus was not increased after coadministration of KA and RPIA. It is consequently suggested that RPIA may attenuate the KA-induced neuronal loss and increase of GFAP immunoreactivity in hippocampus in rats.

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Kainic acid; R-phenylisoprpyladenosine; Hippocampus; GFAP; Epilepsy; Neuroprotection

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