Àá½Ã¸¸ ±â´Ù·Á ÁÖ¼¼¿ä. ·ÎµùÁßÀÔ´Ï´Ù.

Ä®½·, ¸¶±×³×½· ¹× Ä®½· ų·¹ÀÌÆ®°¡ Àú »ê¼Ò ¼Õ»ó ÈÄ ½Å°æ ¼¼Æ÷ ½Ã³À½º Àü´ÞÀÇ È¸º¹¿¡ ¹ÌÄ¡´Â ¿µÇâ Effects of Calcium, Magnesium, and Calcium Chelating Agent on Recovery from Hypoxia in Hippocampal Tissue Slices

´ëÇѽŰæ¿Ü°úÇÐȸÁö 1997³â 26±Ç 4È£ p.491 ~ 498
¼Ò¼Ó »ó¼¼Á¤º¸
±è¿ìÀç/Woo Jae Kim ¹ÚÁ¤À²/¹ÚÀ±°ü/Á¤Èï¼·/À̱âÂù/ÀÌÈÆ°©/Jung Yul Park/Youn Kwan Park/Heung Seob Chung/Ki Chan Lee/Hoon Kap Lee

Abstract

°á ·Ð
°æµµÀÇ Àú»ê¼Ò ¼Õ»ó ÈÄ ÈòÁã Çظ¶Á¶Á÷ÆíÀÇ Schaffer collateral-commissural bundleÀ» Àü
±â ÀÚ±ØÇÏ¿© ¹ß»ýÇÏ´Â population spike¸¦ CAIºÎÀ§¿¡¼­ ÃøÁ¤ÇÏ¿© spikeÁøÆøÀÇ º¯È­¸¦ Àú»ê
¼Ò »óÅ ÈÄ 4½Ã°£±îÁö ÀÏÁ¤ ½Ã°£ °£°ÝÀ¸·Î ±â·ÏÇÏ¿© ´ÙÀ½°ú °°Àº °á·ÐÀ» ¾ò¾ú´Ù.
1) 10ºÐ°£ Àú»ê¼ÒÁõ À¯¹ß ÈÄ ½Å°æ¼¼Æ÷ÀÇ ¹ÝÀÀÀº ¼Ò½ÇµÇ¾ú´Ù.
2) »ê¼Ò Àç°ø±Þ ÈÄ ¹ÝÀÀÀÌ È¸º¹µÇ¸ç óÀ½ 5ºÐ°£ °¡Àå ¸¹ÀÌ È¸º¹µÇ¾ú´Ù. 2½Ã°£ ÀÌÈÄ¿¡´Â
Àú»ê¼ÒÁõÀ» À¯¹ßÇÏÁö ¾ÊÀº À§ ½ÇÇè ´ëÁ¶±º°ú Åë°èÀûÀ¸·Î À¯ÀÇÇÏÁö ¾ÊÀº Á¤µµ·Î ±â´É ȸº¹À»
º¸¿´´Ù.
3) ½Å°æ ±â´É ȸº¹Àº ´ëÁ¶±º¿¡ ºñÇØ Àú³óµµ Ä®½·±º, Àú³óµµ Ä®½·-°í³óµµ ¸¶±×³×½·±º.
BAPTA-AM±º ¸ðµÎ¿¡¼­ ±â´É ȸº¹ÀÇ Çâ»óÀ» º¸¿´°í Àú³óµµ Ä®½·±º¿¡¼­ »ê¼Ò Àç°ø±Þ 5ºÐ
ºÎÅÍ 2½Ã°£±îÁö ´ëÁ¶±ºº¸´Ù Åë°èÀûÀ¸·Î À¯ÀÇÇÑ Â÷À̸¦ º¸¿© 5ºÐºÎÅÍ 60ºÐ±îÁö Åë°èÀû Â÷ÀÌ
¸¦ º¸ÀÎ Àú³óµµ Ä®½·-°í³óµµ ¸¶±×³×½·±ºÀ̳ª 10ºÐ¿¡¸¸ Åë°èÀû Â÷À̸¦ º¸ÀÎ BAFTA-AM±º
º¸´Ù ȸº¹ Á¤µµ°¡ ¿ì¼öÇÏ¿´´Ù.
4) °¢°¢ÀÇ ½ÇÇ豺¿¡¼­ ´ëÁ¶±º¿¡ ºñÇØ »ê¼Ò Àç°ø±Þ ÈÄ 10ºÐ¿¡ °¡Àå Å« ȸº¹Á¤µµÀÇ Â÷À̸¦
º¸¿´´Ù.
5) ¼¼Æ÷¿Ü¾×ÀÇ Ä®½·Àº Àú»ê¼Ò¼º ¼Õ»ó ÈÄ ¼¼Æ÷ÀÇ ±â´É ȸº¹¿¡ ¿µÇâÀ» ÁÖ¾î Àú³óµµ »óųª
Ä®½· È°¼º ÀÌ °¨¼ÒÇÒ ¶§ ȸº¹ÀÌ Çâ»óµÇ¾ú´Ù.
6) ¸¶±×³×½·ÀÇ ³óµµ º¯È­´Â Àú»ê¼Ò ¼Õ»ó ÈÄ Ãʱ⠼¼Æ÷ÀÇ ±â´É ȸº¹¿¡´Â ¿µÇâÀ» ÁÖÁö ¸øÇÏ¿´´Ù.
#ÃÊ·Ï#
To provide an evidence to support the calcium hypothesis of cerebral ischemia, we
examined the effects of the extracellular calcium and calcium chelating
agent(Bapta-AM), and magnesium on in vitro ischemia using rat hippocampal slices.
Loss of the population spike on the hippocampal CA1 region after electrical stimulation
was used as index of damage on the synaptic transmission and spike amplitude of the
population spike as index of recovery level. Recovery from the loss of orthodromic
responses after transient hypoxia in low calcium treated slices was more rapid than
non-treated normal calcium slices, and remained robust for 4 hours in slices exposed in
low calcium, while responses in slices made hypoxic in normal calcium remained
depressed or more slowly recovered. There were statistical significant differences of
amplitude between the two group at 5, 10, 15, 30, 60, 90 and 120 minute after 10 minute
hypoxia(p<0.05). To the lesser extent, similar results was observed in calcium chelating
agent. BAPTA-AM, treated slices, with statistical significant difference at 10 minute
after hypoxia(p<0.05). But in blocker, did not improve recovery compared to reducing
calcium alone. We conclude that recovery from the loss of function after hypoxia was
improved by decreasing extracellular calcium concentration of neurous and activation of
NMDA receptors probably played in early neuronal damage.

Å°¿öµå

Hypoxia; Calcium; Magnesium; BAPTA-AM.;

¿ø¹® ¹× ¸µÅ©¾Æ¿ô Á¤º¸

 

µîÀçÀú³Î Á¤º¸

KoreaMed
KAMS