An electrophysiological study of the action of crude Enhydrina schistosa venom.
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.
D000818:Animals; D002217:Carbachol / Q000494:pharmacology; D004347:Drug Interactions; D005260:Female; D066298:In Vitro Techniques; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D009045:Motor Endplate / Q000187:drug effects / Q000502:physiology; D051381:Rats; D012910:Snake Venoms / Q000494:pharmacology*
D012910:Snake Venoms; D002217:Carbachol