摘要
目的:用鸡胚交感神经元研究3,4-二氨基吡啶(DAP)易化电刺激诱发[~3H]NE释放的机制. 方法:用[~H]NE或fura-2孵育神经元,测[~H]NE释放或[Ca^(2+)]_i. 结果:电刺激诱发[~3H]NE释放和[Ca^(2+)]_i升高被ω-conotoxine GVIA (CTX)抑制,被(—)isradipine(Isp)减弱,被Bay k 8644加强.当3,4-二氨基吡啶(DAP)存在时,电刺激诱发[~3H]NE释放被易化,这时CTX的作用减弱,Isp的作用增强,Bay k 8644不再显示作用. 结论:DAP对电刺激诱发[~3H]NE释放的易化作用,可能是通过L-型Ca^(2+)通道而实现的.
To study the mechanism by which 3,4-diaminopyridine (DAP) facilitates electrically evoked [3H3norepinephrine ([3H]NE) release in sympathetic neurons from chick embryos. METHODS . The neurons were incubated with [3H]NE or Fura-2. [3H]NE release or [Ca21 ], was determined. RESULTS: The electrically evoked C3HHNE release and the elevation of [Ca2+ ]; were inhibited completely by sodium channel blocker tetrodotoxin (TTX), strongly by the antagonist of N-type calcium channel w-conotoxin GVIA (CTX), and slightly by the antagonist of L-type calcium channel ( - ) isradipine > but enhanced by the agonist of L-type calcium channel Bay k 8644. In the presence of DAP, the electrical-ly evoked [3H]NE release and [Ca2+], were facilitated , the inhibition of [3H]NE release and [Ca2+]i by CTX was attenuated, but that by (-)isradipine was enhanced, and Bay k 8644 was no longer effective. CONCLUSION- In the cultured chick sympathetic neurons DAP facilitates electrically evoked [3H]NE release mediated by enhancement of influx of external Ca2+ through the L-type Ca2+ channel.
出处
《中国药理学报》
CSCD
1995年第4期348-351,共4页
Acta Pharmacologica Sinica
基金
Project supported by the Stiftung Volkswagenwerk, Germany and the National Natural Science Foundation of China, №39370237.
关键词
交感神经元
去甲肾上腺素
钙通道
河豚毒素
sympathetic neuron
norepinephrine
3, 4-diaminopyridine
calcium channel
w-conotoxins
tetrodotoxin