Àá½Ã¸¸ ±â´Ù·Á ÁÖ¼¼¿ä. ·ÎµùÁßÀÔ´Ï´Ù.

Kainic Acid À¯¹ß ÈòÁã¹ßÀ۸𵨿¡¼­ (R-)-N6-phenylisopropyladenosineÀÇ Àüóġ°¡ ¹ø¿¬°èÀÇ ½Å°æ¼¼Æ÷Á¢ÂøºÐÀÚ(Netural Cell Adhesion Molecule ; NCAM)ÀÇ ¸é¿ª¹ÝÀÀº¯È­¿¡ ¹ÌÄ¡´Â ¿µÇâ Effect of (R-)-N6-phenylisopropyladenosine (RPIA) Pretreatment on the alteration of Netural Cell dhesion Molecule

´ëÇÑ°£ÁúÇÐȸÁö 1999³â 3±Ç 1È£ p.22 ~ 32
Ȳ¼±Ãâ, Ȳ¼¼Áø, Á¶¿ø±æ, Áøâ¹è, Á¤È£»ï,
¼Ò¼Ó »ó¼¼Á¤º¸
Ȳ¼±Ãâ ( Hwang Seon-Chool ) 
¸Þ¸®³îº´¿ø ½Å°æ°ú

Ȳ¼¼Áø ( Hwang Se-Jin ) 
ÇѾç´ëÇб³ ÀÇ°ú´ëÇÐ ÇغÎ.¼¼Æ÷»ý¹°Çб³½Ç
Á¶¿ø±æ ( Cho Won-Gil ) 
ÇѾç´ëÇб³ ÀÇ°ú´ëÇÐ ÇغÎÇб³½Ç
Áøâ¹è ( Jin Chang-Bae ) 
Çѱ¹°úÇбâ¼ú¿¬±¸¿ø »ýü´ë»ç¿¬±¸¼¾ÅÍ
Á¤È£»ï ( Chung Ho-Sam ) 
ÇѾç´ëÇб³ ÀÇ°ú´ëÇÐ ÇغÎÇб³½Ç

Abstract


Background:Various neuronal and glial factors which participate in neural differentiation, including neural cell adhesion molecule (NCAM), are upregulated in pathogenesis of temporal lobe epilesy (TLE).This study aimed to investigate hte effect of (R-)-N6-phenylisopropyladenosine (RPIA), an adenosine A1 receptor agonist, on the morphological alteration of NCAM immunoreactivity (IR) in limbic system of Kainic acid (KA)-induced epileptic rats.

Methods:Experiment animals were divided into control group, KA treatment only (10 §·/§¸. i.p.)group, and RPIA pretreatment (100 §¶/§¸. i,p, 10 min prior to injection of KA) group. Animals were sacrificed at 24 hours and 1 week after KA treatment. Luxol fast blue-cresyl violet stain for histopathological observation, and NCAM immunohistochemistry to study alteration of NCAM IR in limbic system were performed.

Results:Neuronal loss in CA1 and CA3areas of hippocampus, piridorm cortex, basolateral amygdala nucleus and lateral dorsal thalamic nucleus were induced by KA unjection, and thoes were reduced by RPIA pretreatment. Inrease of NCAM-IR was observed in interneurons of all hippocampal areas. except CA2 area, pirform cortex and basolateral amygdala nucleus at 24 hours after KA injection. and increased NCAM-IR was observed in cell membrane and processes of neuroglia, dentate granule cells and pyramidal cells in CA1 area of hippocampus. and neurons in piriform cortex, amygdala and lateral dorsal thalamic nucleus 1 week after KA injection, but those changes were milder than those at 24 hours after KA injection. RPIA pretreatment significantly reduced KA-induced NCAM-IR in hippocampal CA3, CA1 area, piriform cortex, amtgdala and lateral dorsal thalamic nucleus.

Conclusion:We suggest that decrease of NCAM immunoreactivity is associated with neuprotective effects of RPIA on limbic system against KA neurotoxiciy.

Å°¿öµå

Kainic acid; (R-)-N6-phenylisopropyladenosine ; Limbic system; Netural cell adhesion molecule; Temporal lobe epilepsy

¿ø¹® ¹× ¸µÅ©¾Æ¿ô Á¤º¸

 

µîÀçÀú³Î Á¤º¸

KoreaMed
KAMS