• 作者： 簡伯武
• 作者服務機構： 國立成功大學醫學院藥理學科
• 中文摘要： 4-氨基?啶（4-aminopyridine）已知對中樞扁桃體（Amygdala）神經細胞有引發連續性動作電位及對單一動作電位
  期間有延長作用，而產生癲癇現象。因扁桃體內之神經傳遞物為興奮性氨基酸（excitatory amino acid），所以本實驗將
  利用離體老鼠扁桃體之腦切片作細胞內記錄法，探討興奮性氨基酸感受體阻斷劑對 4-氨基?啶所引發癲癇現象之抑制作
  用。
  Kynuretic acid 隨著劑量之增加能逐漸縮短 4-氨基?啶所引發之癲癇現象。高濃度 Kynuretic acid（1 mM）則能完
  全抑制 4-氨基?啶所引發之癲癇現象。由濃度－反應圖形可推出其為130μM，由另一組實驗發現 NMDA 感受體
  阻斷劑，DL-2-amino-5-phonovalerate 對 4-氨基?啶所引發之癲癇現象並無作用。因此結論：4-氨基?啶所引發之癲癇
  現象和非 NMDA 之興奮性氨基酸有關。.
• 英文摘要： The effects of excitatory amino acid receptor antagonists, kynuretic acid and DL-2-amino-5-pho-sphonovalerate (DL-APV), on spontaneous epileptiform activity induced by 4-aminopyridine (4-AP) werestudied in rat amygdala slices using intracellular recording techniques. Five to ten minutes after switchingto 4-AP containing solution, spontaneous epileptiform bursts were observed in 37 out of 48 slices studied.The spontaneous epileptiform events consisted of an initial burst followed by a number of afterdischarges.Superfusion with kynuretic acid, a nonspecific excitatory amino acid receptor antagonist, reversiblyreduced the duration of the spontaneous bursting discharges in a dose-dependent manner. The frequencyof spontaneous bursting was also decreased. The , estimated from the graph of the concentration-response relationship, was approximately 130 uM. In contrast to kynuretic acid, DL-APV, which is aspecific N-methyl-D-aspartate (NMDA) receptor antagonist, failed to block the spontaneous bursting.These results suggest that activation of excitatory amino acid receptors of non-NMDA type is involved inthe generation or propagation of spontaneous epileptiform events induced by 4-AP in the neurons of baso-lateral amygdala.
• 中文關鍵字： amygdala; 4-aminopyridine; kynuretic acid; brain slices
• 英文關鍵字： --