- 作者: 張傳?; 簡伯武
- 作者服務機構: 臺灣大學醫學院藥理研究所
- 中文摘要: 為要探討運動神經末端之ACh感受體是否有迴饋調節神經傳遞物質釋放之功能,本篇以微細電極細胞內記錄法,在小鼠膈神經-橫膈膜肌肉標本研究Carbachol, d-tubocnrarine, α-bungar6toxinRatropine對自發性微小終板電位(m.e.p.p.)之頻率及神經刺激引發終板電位(e.p.p.)量子數含量之影響。 Carbachol於5.5 × 10 M時可毀極化終板部位靜止膜電位約7mv, m.e.p.p.高度亦減少3成但m.e.p.p.頻率則自1.4/sec增加6成到2.2/sec.這些作用均可維持相當長時間(50min),未見有Desensitization現象,洗去Carbachol時其數值均迅速恢復。Atropine,d-tubocurarine,α-bungarotoxin本身對正常標本則不改變m.e.p.p.頻率。但Carbachol所引起m.e.p.p.頻率之變化可用極少量d-tubocurarine或α-bungarotoxin所對抗,但Atropine則不能對抗之。可見Carbachol引起之變化係作用於Nicotinic 型ACh感受體之結果。在高濃度鎂(7.7mM)存在下,以0.5Hz刺激引發e.p.p.時Carbachol對e.p.p.所含量子數並無影響。pfd-tubocurarine遮斷神經-肌傳導之標本若以50Hz刺激引發一系列e.p.p.時其高度以次降低,Carbachol對此一系列e.p.p.之次降低情形亦無改變作用,表示Carbachol對神經傳遞物質之釋放,貯存及輸送並無影響。Carbachol增加m.e.p.p.之頻率可能由對運動神經末端ACh感受體作用而毀極化之結果而產生,但此ACh感受體在生理學上似無有效調節運動神經末端釋放之功能。
- 英文摘要: The effects of carbachol, d-tubocurarine, α-bungarotoxin and atropine on the frequency of spon-taneously occurring miniature endplate potentials (m.e.p.p.)and quantal contents of endplate potentials(e.p.p.)evoked by low and high frequency stimulations in the isolated mouse phrenic nervediaphragmpreparation were studied in order to shed more light on the possible physiological function of acetylcholinereceptors (AChR) in regulating the release of neurotransmitters from the motor nerve terminal. Carbachol,at a concentration of (5.5 × 10 M), which depolarized the membrane potential at the endplate area byabout 7 mV, decreased the mean amplitude of m.e.p.p.s but increased the frequency of m.e.p:p.s by about60%. These effects appeared quickly after addition of carbachol and were sustained for more than 50 min.They were reversible upon washing. These effects produced by using carbachol were not antagonized byatropine but were completely antagonized by d-tubocurarine and α-bungaro-toxin at low concentrationsfar below that necessary for blocking neuromuscular transmission. These two antagonists, however, didnot change the m.e.p.p. frequency of normal preparations not treated with carbachol. On the other hand,the quantal content of e.p.p.s evoked at 0.5 Hz in the p=esence of high Mg concentration was notaffected by carbachol. Furthermore, the successive decline of e.p.p.s during training stimulations at 50 Hzwas not changed, indicating that carbachol has no effect on the release, storage and mobilization ofneurotransmitter. The increase of m.e.p.p. frequency as a result of using carbachol may be due to a simpledepolarization caused by an action of the nicotinic AChR on the nerve terminal. It can be concluded thatthe AChR on the nerve terminal of mice plays no important role in the feedback control of transmitterrelease.
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