Transmitter releasing action of selegiline ((—)‐deprenyl) from peripheral sympathetic nerves under different experimental conditions
Transmitter releasing action of selegiline ((—)‐deprenyl) from peripheral sympathetic nerves under different experimental conditions
复制标题
不同实验条件下周围交感神经司来吉兰（(—)-丙炔苯丙胺）递质释放作用
DOI：
10.1111/j.2042-7158.1987.tb05121.x
复制
发表时间：
1987
影响因子：
3.3
通讯作者：
K. Magyar
中科院分区：
文献类型：
--
作者：
T. Török;Tünde Pauló;P. Tóth;T. Nguyen;A. M. Azzidani;K. Magyar
在神经元（可卡因，3 倍 10−5M）和神经元外（皮质酮，5 倍 10−5M）摄取阻滞剂存在的情况下，高浓度司来吉兰（(—)-丙炔苯丙胺；10−4M）增强低频（2 Hz）神经刺激诱发兔子离体主肺动脉释放[3H]去甲肾上腺素，并抑制突触后反应。 10−4M 司来吉兰的递质释放作用受到适度增加的外部 K+ (23ṁ6mM) 的抑制。过量的 K+ 本身消除了[3H]去甲肾上腺素的神经诱发释放，但并没有增加静息放射性流出。过量的 Ca2+ (7ṁ mM) 增加了刺激诱发的递质释放。在存在过量 Ca2+ 的情况下，司来吉兰 (10−4M) 可有效增加响应神经刺激的 [3H] 去甲肾上腺素释放。过量的 Ca2+ 部分拮抗司来吉兰的突触后抑制作用。在不含 Ca2+、含 1 mM EGTA 的 Krebs 溶液中，神经诱发的 3H 释放和司来吉兰的递质释放作用均被消除，与“Ca 假说”一致。电压依赖性 K+ 通道阻滞剂 4-氨基吡啶 (10-5M) 可增加神经刺激诱发的动脉氚释放。如果灌注介质中也存在司来吉兰，则神经诱发的递质释放进一步增加。 4-氨基吡啶完全拮抗司来吉兰对突触后收缩的抑制作用。
A high concentration of selegiline ((—)‐deprenyl; 10−4M) potentiated low frequency (2 Hz) nerve stimulation‐evoked release of [3H]noradrenaline from the isolated main pulmonary artery of the rabbit in the presence of neuronal (cocaine, 3 times 10−5M) and extraneuronal (corticosterone, 5 times 10−5M) uptake blockers, and inhibited the postsynaptic response. The transmitter‐releasing action of 10−4M selegiline was inhibited by a moderate increase of external K+ (23ṁ6mM). Excess K+ by itself abolished the nerve‐evoked release of [3H]noradrenaline but did not increase the resting outflow of radioactivity. Excess Ca2+ (7ṁ mM) increased the stimulation‐evoked transmitter release. In the presence of excess Ca2+, selegiline (10−4M) was effective in increasing the [3H]noradrenaline release in response to nerve‐stimulation. Excess Ca2+ partly antagonized the postsynaptic inhibitory action of selegiline. In Ca2+‐free, 1 mM EGTA‐containing Krebs solution both the nerve‐evoked 3H release and the transmitter releasing action of selegiline were abolished, in agreement with the ‘Ca‐hypothesis’. The voltage‐dependent K+‐channel blocker, 4‐ami‐nopyridine (10−5M), increased the nerve‐stimulation‐evoked release of tritium from arteries. If selegiline was also present in the perfusion medium the nerve‐evoked transmitter release further increased. 4‐Aminopyridine completely antagonized the inhibitory action of selegiline on the postsynaptic contraction.