- 作者: 蔡明正
- 作者服務機構: 國立臺灣大學醫學院藥理學研究所
- 中文摘要: 本文利用電生理學之方法,研究非洲大蝸牛中樞神經細胞(舌下神經節TAN細胞)動作電位之離子需要性。 在正常蝸牛溶液內,刺激大蝸牛中樞神經細胞可引起動作電位。在缺鈣離子之蝸牛溶液內,刺激神經細胞並不產生動作電位。鈣之抑制劑Verapamil也可抑制神經細胞動作電位之幅度(Amplitude)及上升速率(Vmax)。顯示此動作電位與鈣離子有關。在缺鈉離子之蝸牛溶液內,神經細胞動作電位之幅度及上升速率也被抑制。但是鈉離子通道之抑制劑-河豚毒素(Tetrodotoxin),卻不影響神經細胞動作電位之幅度及上升速率。由以上實驗結果顯示,非洲大蝸牛中樞神經細胞之動作電位與鈉離子及鈣離子有關。其鈉離子通道與一般之骨骼肌,神經之Tetrodotoxin-sensitive鈉通道不同。而大蝸牛中樞神經動作電位可能主要係經由鈣離子而來。
- 英文摘要: The ionic requirement for the production of directly elicited action potentials of a tonically auto-active neuron (TAN) in the subesophageal ganglia of the giant African snail, Achatina fulica Ferussac, wasstudied electrophysiologically. Calcium free Ringer solution containing 1 mM EDTA reversibly abolishedthe directly elicited action potential. Verapamil (10 μg/ml) or cocaine (4 μg/ml) decreased both amplitudeand Vmax of the action potentials. The amplitude of the action potential was also slightly decreased insodium free choline Ringer. However, tetrodotoxin did not significantly affect either the amplitude orVmax of the directly elicited action potentials. The results suggest that the ionic requirement, for generatingaction potential in snail neuron is not an ordinary sodium spike. Both calcium and sodium ions may par-ticipate in carrying charges across the membrane of the action potential.
- 中文關鍵字: gastropod central neuron; action potential
- 英文關鍵字: --