The potassium current blockers caesium and tetraethylammonium were injected intracellularly by ionophoretic current into brainstem expiratory neurones of the ventral group. Neurones were identified by their spontaneous activity and by antidromic excitation from the spinal cord at the C2-C3 level. 2. The duration of action potentials increased and the early and late after-hyperpolarizations were completely suppressed. These effects on action potentials were reversible, recovered with an exponential time course within 3 min, and could be reproduced when blockers were applied repetitively into the same neurone. They were ascribed to blockade of potassium channels in the somatic membrane region. 3. Potassium channel blockers modified postsynaptic potentials: early-inspiratory hyperpolarizations were reversibly depressed while postinspiratory and expiratory depolarizations were irreversibly enhanced. The former effect was associated with a decrease of the neuronal input conductance. The latter effect was cumulative upon repetitive ionophoretic applications of potassium blockers. 4. The results demonstrate that potassium currents exert two different roles in expiratory pattern generation. Together with chloride currents, they contribute to the phasic early-inspiratory inhibition. They seem to be calcium-dependent and GABAB receptor-controlled currents which predominate near to the cell body. 5. Potassium currents also operate throughout the postinspiratory and late-expiratory periods. They seem to include persistent potassium currents which modulate the excitatory respiratory drive provided by the respiratory rhythm generator. We assume that these currents, widely distributed over the somatodendritic membrane area, are a target for neuromodulation by transmitters and intracellular second messengers.
