1. Respiratory neurons of mammals are rhythmically active because their membrane potential fluctuates periodically over a voltage range of -70 to -55 mV. These respiratory drive potentials lead to periodic discharges of bursts of action potentials lasting for 1-2 s. The neuronal processes stabilizing this rhythmic activity involve excitatory and inhibitory synaptic processes that interact with specific membrane properties of the postsynaptic neurones. In the present experiments, performed on dorsal and ventral groups of respiratory neurones under in vivo and in vitro conditions, we verified the modulating feature of such intrinsic neuronal properties. 2. Intrinsic neuronal properties involve Ca2+ mechanisms that lead to intracellular Ca2+ accumulation, and consequently to activation of Ca(2+)-dependent K+ currents. 3. Blockade of intracellular Ca2+ accumulation significantly changed the amplitude and pattern of respiratory drive potentials, and blocked initial hyperpolarizing shifts of the membrane potential following each period of synaptic activation. 4. The data demonstrate that postsynaptic activities and action potential discharges activate low and high voltage-activated Ca2+ currents leading to intracellular Ca2+ accumulation and to activation of Ca(2+)-dependent K+ currents that significantly modulate the voltage response of medullary respiratory neurones to on-going synaptic activation. These intrinsic membrane properties also seem to be involved in the processes controlling termination of rhythmic burst discharges.