NO decreases evoked quantal ACh release at a synapse of Aplysia by a mechanism independent of Ca2+ influx and protein kinase G.
NO decreases evoked quantal ACh release at a synapse of Aplysia by a mechanism independent of Ca2+ influx and protein kinase G.
复制标题
NO 通过独立于 Ca2 流入和蛋白激酶 G 的机制减少海兔突触处诱发的量子 ACh 释放。
DOI：
10.1113/jphysiol.1996.sp021421
复制
发表时间：
1996
期刊：
影响因子：
--
通讯作者：
G. Baux
中科院分区：
文献类型：
--
作者：
J. Mothet;P. Fossier;L. Tauc;G. Baux
1.外源性一氧化氮（NO）供体SIN-1降低了由突触前锋电位诱发的突触后反应，该突触前锋电位位于加利福尼亚蝙蝠的颊神经节中的已识别胆碱能神经元-神经元突触处。2.对电压钳位突触前神经元的方形去极化诱发的长持续时间突触后反应的统计分析表明，SIN-1减少了诱发的乙酰胆碱（ACh）量子释放的数量，表明药物具有突触前作用。3.维生素E是一种自由基清除剂，可以阻止SIN-1对ACh释放的影响。SIN-1在超氧化物歧化酶的存在下仍然减少ACh的释放，而血红蛋白抑制SIN-1的作用。这些结果表明NO是活性化合物。4. 8-溴鸟苷3 '，5'环一磷酸（8-Br-cGMP）模拟NO对ACh释放的抑制作用，表明NO敏感性鸟苷酸环化酶的参与。鸟苷酸环化酶、亚甲蓝、胱胺或LY 83583抑制剂对SIN-1作用的可逆性加强了这一点。亚甲基蓝可部分降低NO对ACh释放的抑制作用。此外，在超氧化物歧化酶存在下，亚甲基蓝可阻断NO对ACh释放的抑制作用，胱胺可显著降低NO对ACh释放的抑制作用。5.在存在KT 5823或R-p-8-pCPT-cGMPS（两种蛋白激酶G抑制剂）的情况下，SIN-1仍能减少ACh释放，表明NO的作用很可能不涉及蛋白激酶G依赖性磷酸化。6.突触前电压依赖性Ca 2+（L-、N-和P-型）和K+（IA和晚期外向整流）电流未被SIN-1改变。7. L-精氨酸和N-ω-硝基-L-精氨酸以相反的方式调节ACh释放，表明内源性NO合酶依赖性调节递质释放。
1. The exogenous nitric oxide (NO) donor, SIN‐1, decreased the postsynaptic response evoked by a presynaptic spike at an identified cholinergic neuro‐neuronal synapse in the buccal ganglion of Aplysia californica. 2. The statistical analysis of long duration postsynaptic responses evoked by square depolarizations of the voltage‐clamped presynaptic neurone showed that the number of evoked acetylcholine (ACh) quanta released was decreased by SIN‐1, pointing to a presynaptic action of the drug. 3. Vitamin E, a scavenger of free radicals, prevented the effects of SIN‐1 on ACh release. SIN‐1 still decreased ACh release in the presence of superoxide dismutase, whereas haemoglobin suppressed the effects of SIN‐1. These results showed that NO is the active compound. 4. 8‐Bromoguanosine 3', 5' cyclic monophosphate (8‐Br‐cGMP) mimicked the inhibitory effect of NO on ACh release suggesting the involvement of a NO‐sensitive guanylate cyclase. This was reinforced by the reversibility of the effects of SIN‐1 by inhibitors of guanylate cyclase, Methylene Blue, cystamine or LY83583. Methylene Blue partially reduced the inhibitory effect of NO. In addition, in the presence of superoxide dismutase, Methylene Blue blocked and cystamine significantly reduced the NO‐induced inhibition of ACh release. 5. In the presence of KT5823 or R‐p‐8‐pCPT‐cGMPS, two inhibitors of protein kinase G, the reduction of ACh release by SIN‐1 still took place indicating that the effects of NO most probably did not involve protein kinase G‐dependent phosphorylation. 6. Presynaptic voltage‐dependent Ca2+ (L‐, N‐ and P‐types) and K+ (IA and late outward rectifier) currents were unmodified by SIN‐1. 7. The modulation of ACh release in opposite ways by L‐arginine and N omega‐nitro‐L‐arginine points to the involvement of an endogenous NO synthase‐dependent regulation of transmitter release.
DOI：
--
发表时间：
1985-03
期刊：
The Journal of pharmacology and experimental therapeutics
影响因子：
--
作者：
W. Martin;G. Villani;D. Jothianandan;R. Furchgott
通讯作者：
W. Martin;G. Villani;D. Jothianandan;R. Furchgott
亚甲蓝通过细胞外产生超氧阴离子来抑制骨骼肌小动脉向乙酰胆碱和一氧化氮的血管舒张。
DOI：
--
发表时间：
1990
期刊：
The Journal of pharmacology and experimental therapeutics
影响因子：
--
作者：
Wolin,MS;Cherry,PD;Rodenburg,JM;Messina,EJ;Kaley,G
通讯作者：
Kaley,G
DOI：
10.1073/pnas.87.4.1620
发表时间：
1990-02-01
影响因子：
11.1
作者：
BECKMAN, JS;BECKMAN, TW;FREEMAN, BA
通讯作者：
FREEMAN, BA