The inferior colliculus (IC) is a major center for neural integration in the auditory pathway. The IC processes inputs from the lower brainstem as well as from higher centers in the auditory system. To understand cellular mechanisms of IC neurons in auditory processing, we investigated physiological characteristics of the rebound depolarization (RD) following membrane hyperpolarization in neurons of the rat's dorsal cortex of the inferior colliculus (ICD). Whole-cell patch clamp recordings were made from ICD neurons in brain slices. In more than half of the ICD neurons, there was a RD accompanied by one or two anode break action potentials (APs) following membrane hyperpolarization. The RD was Ca(2+) mediated and primarily due to activation of low-threshold T-type Ca(2+) channels. Generation of the RD and anode break APs depended on the magnitude and duration of the preceding hyperpolarization. Larger and longer hyperpolarization induced a larger, shorter and faster rebound, and therefore earlier anode break APs. However, with further hyperpolarization the RD became constant in amplitude and duration despite increases in the strength or duration of the preceding hyperpolarization. Usually, membrane hyperpolarization as small as -15 mV for 100-200 ms was enough to induce a pronounced rebound of 15-20 mV. The RD in IC neurons may provide a neuronal mechanism for integrating excitatory inputs arriving soon after a period of synaptic inhibition and therefore processing specific aspects of auditory information.