Humans effortlessly interpret speech and music, whose patterns can contain sound durations up to thousands of milliseconds. How nervous systems measure such long durations is unclear. We show here that model neurons containing physiological slow conductances are 'naturally' sensitive to duration, replicate known duration-sensitive neurons and can be 'tuned' to respond to a wide range of specific durations. In addition, these models reproduce several other properties of duration-sensitive neurons not selected for in model construction. These data, and the widespread presence of slow conductances in nervous systems, suggest that slow conductances might play a major role in duration measurement.

Humans effortlessly interpret speech and music, whose patterns can contain sound durations up to thousands of milliseconds. How nervous systems measure such long durations is unclear. We show here that model neurons containing physiological slow conductances are 'naturally' sensitive to duration, replicate known duration-sensitive neurons and can be 'tuned' to respond to a wide range of specific durations. In addition, these models reproduce several other properties of duration-sensitive neurons not selected for in model construction. These data, and the widespread presence of slow conductances in nervous systems, suggest that slow conductances might play a major role in duration measurement.

The rhythmic pyloric network of the lobster stomatogastric system approximately maintains phase (that is, the burst durations and durations between the bursts of its neurons change proportionally) when network cycle period is altered by current injection into the network pacemaker (Hooper, 1997a,b). When isolated from the network and driven by rhythmic hyperpolarizing current pulses, the delay to firing after each pulse of at least one network neuron type [pyloric (PY)] varies in a phase-maintaining manner when cycle period is varied (Hooper, 1998). These variations require PY neurons to have intrinsic mechanisms that respond to changes in neuron activity on time scales at least as long as 2 s. Slowly activating and deactivating conductances could provide such a mechanism. We tested this possibility by building models containing various slow conductances. This work showed that such conductances could indeed support intrinsic phase maintenance, and we show here results for one such conductance, a slow potassium conductance. These conductances supported phase maintenance because their mean activation level changed, hence altering neuron postinhibition firing delay, when the rhythmic input to the neuron changed. Switching the sign of the dependence of slow-conductance activation and deactivation on membrane potential resulted in neuron delays switching to change in an anti-phase-maintaining manner. These data suggest that slow conductances or similar slow processes such as changes in intracellular Ca 2ϩ concentration could underlie phase maintenance in pyloric network neurons.