Electrophysiological studies on the heart of the bivalve mollusc, Modiolus demissus. II. Ionic basis of the action potential.

Investigations concerning the ionic basis of the action potential in nerve and muscle have revealed a variety of mechanisms ranging from total dependence on sodium, first described quantitatively in the squid axon (Hodgkin & Huxley, 1952), to total dependence on calcium in crustacean muscles (Fatt & Ginsborg, 1958; Abbott & Parnas, 1965; Hagiwara & Naka, 1964; Hagiwara & Nakajima, 1966). Between these extremes, various combinations of sodium and calcium conductances comprise spike-generating mechanisms. For example, calcium and other divalent cations produce spike currents in the absence of sodium, although in normal bathing solutions sodium is the principle source of current (Tasaki, Watanabe & Singer, 1966; Gerasimov, Kostyuk & Maiskii, 1965; Koketsu & Nishi, 1969). In some instances, however, action potentials occurring for several hours in Na-free solutions appear to depend on stores of sodium ions trapped at the surface of the membrane (Chamberlain & Kerkut, 1967; Moreton, 1968; Carlson & Treherne, 1969). A variety of intermediate examples have been described where both sodium and calcium carry the spike currents (Geduldig & Junge, 1968), where the proportions of the two ions involved vary with the membrane potential (Irisawa, Irisawa & Shigeto, 1969), and where one or more ions are associated with specific components of the action potential. The latter category shows a rich diversity among vertebrate hearts. Sodium has been associated principally with rise time and overshoot of the action potential (Draper & Weidmann, 1951; Brady & Woodbury, i960; Weidmann, 1955), although calcium also contributes to the spike in some instances (Niedergerke & Orkand, 1966; Matsubara & Matsuda, 1969). Lack of, or interference by, manganese or calcium also blocks the spike plateau (Hagiwara & Nakajima, 1966; Gamier et al. 1969; Yanaga & Holland, 1969), although Gamier et al. (1969) demonstrated that under certain conditions the plateau amplitude was dependent on external sodium. Although the contributions of sodium cannot be entirely discounted, calcium appears to be the major current source in visceral smooth muscle (Holman, 1958; Bulbring & Kuriyama, 1963; Nonomura, Hotta & Ohashi, 1966; Brading, Bulbring & Tomita, 1969).