1. Electrical and mechanical properties of the red muscle (M. levator pinnae pectoralis) and white muscle (M. levator pinnae lateralis abdominis) in the silver carp (Carassius auratus Linné) were investigated by using caffeine and thymol.
2. A complete tetanus could be produced in the red muscle. But in the white muscle no tetanus was produced and there was a gradual decrease in tension during continuous stimulation, even at a frequency of 1 c/s or less.
3. Caffeine (0.5-1 mM) and thymol (0.25-0.5 mM) potentiated the twitch tension in both muscles without an increase in the resting tension; they produced a contracture in both muscles when the concentration was increased further.
4. The falling phase of the active state of contraction was nearly the same in both muscles and was prolonged by caffeine (0.5 mmM) and by thymol (0.25 mM).
5. The resting membrane potential of the red muscle was scarcely affected by caffeine (0.5-5 mM), whereas in the white muscles a depolarization of 10 mV was observed with caffeine of more than 2 mM. The resting potential of both muscles was little changed by o.25 mm thymol. However, at a concentration of more than 0.5mM thymol depolarized the membrane in both muscles to the same extent.
6. In caffeine (2-3 mM) solution the mean specific membrane resistance was reduced from 8.8 kΩ cm2 to 6.0 kΩ cm2 in the red muscle, and from 5.0 kΩ cm2 to 2.7 kΩ cm2 in the white muscle. In thymol (0.5-1 mM) solution it was reduced from 11.2 kΩcm2 to 6.5 kΩ cm2 in the red muscle, and from 5.4kΩ cm2 to 3.1 kΩ) cm2 in the white muscle. The specific membrane capacitance, calculated from the time constant and the membrane resistance, remained more or less the same in both muscles after a treatment with these agents.
7. Electrical properties of the muscles and the effects of caffeine and thymol on mechanical responses suggest that there are no fundamental differences between red and white muscles except for the excitation-contraction coupling. A lack of summation of twitch, a successive decline of twitch, and inability to produce potassium contracture in the white muscle may be due to the fact that the Ca-releasing mechanism is easily inactivated by depolarization of the membrane.