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1. A method which permitted control of the membrane potential near the end of a muscle fibre and measurement of an approximation of the membrane current was used to investigate the effects of the tetraethylammonium (TEA) ion on the delayed outward potassium current obtained on depolarizing.

2. Assuming R_i to be 250 cm and a fibre diameter of 80 µ, the mean value for the maximum potassium conductance (_K) was 23·2 ± 3·2 mmho.cm^-2.

3. 58 mM-TEA, in two series of experiments, reduced _K by about 90%. A concentration—effect relation for TEA in its action on the delayed rectifier could be fitted by a curve for a drug-receptor complex assuming one molecule of TEA to combine reversibly with one receptor, and a dissociation constant of 8 x 10^-3 M.

4. TEA tended to shift the threshold for delayed rectification to slightly more negative membrane potentials. TEA caused a similar shift in the relation between n and membrane potential, but did not much alter the form of the relation.

5. The relation between n and membrane potential and between _n^-1 and membrane potential were well fitted by the model of Adrian, Chandler & Hodgkin (1970a) assuming that the Q₁₀ was 2·5.

6. TEA slowed the rate of onset of the delayed potassium currents, decreasing _n^-1 (the reciprocal of the time constant of the fourth power function which described the current's development) by about 80%.

7. The inactivation of the delayed current with time was shown to follow a complex time course. A fast phase decays with a time constant of 270 msec and a slow phase with a time constant of 2·3 sec at a membrane potential of + 10 mV.

8. The fast phase of the delayed current is much more susceptible to the action of TEA than the slow phase, and these are interpreted in terms of different potassium channels. TEA has little effect on the time constant with which either the fast current or the slow current inactivates.