Ferry C B, Geh S L
Br J Pharmacol. 1977 Jun;60(2):233-8. doi: 10.1111/j.1476-5381.1977.tb07745.x.
1 Electrophysiological studies on the rat diaphragm revealed that crude Enhydrina schistosa venom has a blocking action on postjunctional acetylcholine (ach) receptors. 2 This venom in concentrations of 0.125-1.0 microgram/ml abolished the extracellular endplate potential (e.e.p.p.) without altering the presynaptic spike. When the phrenic nerve was stimulated at a frequency of 1 Hz the degree of depression of successive e.e.p.ps was approximately the same in records made before and after treatment with venom. 3 In concentrations of 0.25 and 0.5 microgram/ml the venom reduced significantly the amplitude of miniature endplate potentials (m.e.p.ps). The frequency of m.e.p.ps did not increase but was decreased when the amplitue of the m.e.p.ps was much reduced. 4 The crude venom did not alter the resting membrane potential (RMP) of the muscle cell. 5 The venom inhibited the depolarization of the muscle membrane caused by carbachol. 6 It is concluded that an active component in the crude venom is responsible for a blocking action on postjunctional receptors.
1 对大鼠膈肌的电生理研究表明,粗海蛇毒对突触后乙酰胆碱(ACh)受体具有阻断作用。2 这种浓度为0.125 - 1.0微克/毫升的毒液可消除细胞外终板电位(e.e.p.p.),而不改变突触前峰电位。当以1赫兹的频率刺激膈神经时,在用毒液处理前后所记录的连续e.e.p.p.s的抑制程度大致相同。3 浓度为0.25和0.5微克/毫升时,毒液显著降低了微小终板电位(m.e.p.p.s)的幅度。当m.e.p.p.s的幅度大幅降低时,其频率并未增加反而降低。4 粗毒液未改变肌肉细胞的静息膜电位(RMP)。5 毒液抑制了卡巴胆碱引起的肌肉膜去极化。6 得出的结论是,粗毒液中的一种活性成分对突触后受体具有阻断作用。