Maas A J, Den Hertog A
Eur J Pharmacol. 1979 Sep 15;58(2):151-6. doi: 10.1016/0014-2999(79)90006-2.
The polypeptide apamin caused a small depolarization of the muscle cell membrane of the guinea-pig taenia coli accompanied by enhancement of spike activity and a concomitant muscle contration. The membrane hyperpolarization evoked by intramural stimulation of the non-adrenergic inhibitory nerves (inhibitory junction potential) was reduced by apamin; the antagonism being non-competitive in nature. The rebound depolarization and contraction following the inhibitory junction potential was enhanced by apamin. The membrane hyperpolarization induced by the purinergic compound ATP and by the sympathomimetic adrenaline was converted to a depolarization in the presence of apamin. This depolarization resulted in an increased spike activity and muscle contraction. This was followed by membrane hyperpolarization and muscle relaxation after washout of the drugs. These findings indicate that apamin is a non-competitive, non-specific antagonist of the non-adrenergic inhibitory transmitter and that the inhibitory junction potential and the rebound are mutually independent phenomena.
多肽蜂毒明肽可引起豚鼠结肠带肌细胞膜出现微小的去极化，同时伴有锋电位活动增强及随之而来的肌肉收缩。蜂毒明肽可降低由壁内非肾上腺素能抑制神经刺激诱发的膜超极化（抑制性接头电位）；这种拮抗作用本质上是非竞争性的。蜂毒明肽可增强抑制性接头电位后的反冲去极化和收缩。在蜂毒明肽存在的情况下，嘌呤能化合物ATP和拟交感神经药肾上腺素诱导的膜超极化转变为去极化。这种去极化导致锋电位活动增加和肌肉收缩。药物洗脱后，随之出现膜超极化和肌肉松弛。这些发现表明，蜂毒明肽是非肾上腺素能抑制性递质的非竞争性、非特异性拮抗剂，并且抑制性接头电位和反冲是相互独立的现象。
