SUMMARY1. Electrical constants were determined on isolated single fibres or on fibres from bundles from frog's twitch muscles by analyzing the low frequency cable properties.2. The sarcoplasmic conductivity (GQ) was 5 9 mmho/cm at 20°C, and its temperature coefficient (Q10) was 1-37.3. The Q10 of the membrane conductance (GM) was 1-49, and that of the membrane capacity (CM) was 1-02. CM increases with diameter (D) in an approximately linear manner:the values were 4-6 /XF/cm2 at D = 50 ,t, and 8.5 ,#F/cm2 at D = 130 ec.5. GM also increases with diameter, being 0-21 mmho/cm2 at D = 50It and 0 37 mmho/cm2 at D = 130 It.6. These results suggest that the transverse tubular system contributes substantially to the values of low frequency capacity and conductance measured at the surface membrane.

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The effects of tetrodotoxin, procaine, and manganese ions were examined on the Ca spike of the barnacle muscle fiber injected with Cabinding agent as well as on the action potential of the ventricular muscle fiber of the frog heart. Although tetrodotoxin and procaine very effectively suppress the "Na spike" of other tissues, no suppressing effects are found on "Ca spike" of the barnacle fiber, while the initiation of the Ca spike is competitively inhibited by manganese ions. The initial rate of rise of the ventricular action potential is suppressed by tetrodotoxin and procaine but the plateau phase of the action potential is little affected. In contrast the suppressing effect of manganese ions is mainly on the plateau phase. The results suggest that the plateau phase of the ventricular action potential is related to the conductance increase in the membrane to Ca ions even though Na conductance change may also contribute to the plateau.Spike potentials of most excitable tissues such as the squid giant axon (Hodgkin and Katz, 1949) and the skeletal muscle fiber of the frog (Nastuk and Hodgkin, 1950) are believed to occur as a result of an increase in Na ion conductance of the membrane followed by an increase in K conductance. In contrast to this, the spike potential of some crustacean muscle fibers is produced by an increase in the membrane conductance to Ca ions; this is also followed by an increase of K conductance. The latter type of spikes can, therefore, be called the " C a spike" and the former the " N a spike." The Ca spike was demonstrated in a crayfish muscle fiber by Fatt and Ginsborg (1958), Parnas and Abbott (1964), and in barnacle muscle fiber with low internal Ca++ concentration by Hagiwara and Naka (1964). In the action potential of the frog heart ventricle, the rapid depolarization seems to be due to an increase in Na conductance, 793

SUMMARY1. Two types of after-potentials in the stretch receptor neurone of crayfish are described.2. A short-duration after-hyperpolarization associated with a single spike or a few spikes is diminished and reversed on applying hyperpolarizing currents. However, a much longer-lasting post-tetanic hyperpolarization (PTH) is enhanced by conditioning hyperpolarization; thus, no reversal potential can be obtained.3. No changes in membrane conductance occur during PTH. 4. Reducing K concentration in the bathing fluid diminishes PTH, while it shifts the reversal potential of the short after-potential toward greater negativity.5. Replacement of Na with Li, or addition of 2,4-dinitrophenol in the bathing fluid suppresses PTH in a reversible manner.6. Electrophoretic injection of Na into the cell induces a long-lasting hyperpolarization.7. No change in K-equilibrium potential, as indicated by the reversal point of the short after-potential, is detected during PTH.8. It is concluded that the short after-potential is caused by a permeability increase for potassium ion, whereas PTH is produced by an electrogenic Na-pump.

Voltage clamp analyses, combined with pharmacological tools demonstrate the independence of reactive Na and K channels in electrically excitable membrane of eel electroplaques. Spike electrogenesis is due to Na activation and is eliminated by tetrodotoxin or mussel poison, or by substituting choline, K, Cs, or Rb for Na in the medium. The K channels remain reactive, but K activation is always absent, the electroplaques responding only with K inactivation. This is indicated by an increased resistance when the membrane is depolarized by more than about 30 mv. The resting resistance (1 to 5 ohm cm 2 ) is dependent upon the ionic conditions, but when K inactivation occurs the resistance becomes about 10 ohm cm 2 in all conditions. K inactivation does not change the EMF significantly. The transition from low to high resistance may give rise to a negative-slope voltage current characteristic, and to regenerative inactivation responses under current clamp. The further demonstration that pharmacological K inactivation (by Cs or Rb) leaves Na activation and spike electrogenesis unaffected emphasizes the independence of the reactive processes and suggests different chemical compositions for the membrane structures through which they operate.An observation by Altamirano (1955) implied that the intracellularly recorded spikes of eel electroplaques differ from the conductile responses of most other cells. The resistance of the electrogenically reactive caudal membrane of the electroplaques increased two-to threefold over the resting value when this membrane was depolarized by applied currents which exceeded a certain threshold. The increase was evident during the falling phase of the spikes which were elicited by the applied currents and it persisted as long as the current pulses were applied (ca. 20 msec.). The resistance increase also