It is now well established (43, 44, 79, 157, 183) that physiological contraction of skeletal muscle is elicited by calcium ion released from the sarcoplasmic reticulum (SR). The molecular mechanism of how the released calcium ion triggers off the contractile reaction, the myosin-actin interaction, also has been worked out fairly well (41, 43, 44). In the absence of calcium ion, the regulatory proteins of vertebrate striated muscles, troponin and tropomyosin, exert an inhibitory effect on actin so that the actin-myosin interaction is prevented. Troponin, which consists of three nonindentical subunits, troponin T, troponin I, and troponin C, is the receptor protein for calcium. Thus, the calcium ion released binds to one of the troponin subunits, troponin C, and the resulting changes in conformational state of the regulatory proteins remove the inhibition, enabling the contractile reaction to start1 On the other hand, the mechanism of calcium ion release from the SR is much less well understood. The physiological stimulus causing release of calcium is depolarization of the surface membrane, which usually takes the form of an action potential in ordinary twitch fibers. The action potential is conducted from the surface deeply into the muscle cell through the transverse molluscan and some other invertebrate muscles, calcium was found to interact with myosin (114)