Coronal brain slices from 21–50-d-old hooded rats were used to characterize intracellular responses of cells in both the external and dorsal cortices of the inferior colliculus (IC). These cells could generate both sodium and calcium spikes. Depending on current amplitude, depolarizing current pulses could elicit either phasic or tonic firing patterns, with spike frequency adaptation. Spiking also occurred at the offset of a hyperpolarizing pulse. These patterns were due primarily to the activation of calcium conductances. Stimulation of the commissural pathway connecting the left and right IC produced a short-latency monosynaptic IPSP followed by an EPSP(s) and a late polysynaptic IPSP(s). Non-NMDA glutamate antagonists eliminated or reduced the amplitude of the EPSP and the late portion of the inhibition, while both IPSPs were blocked by GABAA antagonists. As described previously in guinea pig (Smith, 1986) and rat (Pierson et al., 1989), a large NMDA-mediated depolarizing event (paroxysmal depolarizing shift, or PDS) could be elicited by shocking the commissure of the IC in the presence of picrotoxin or bicuculline, NMDA, 4-aminopyridine, or in 0 Mg2+ Ringer's. The picrotoxin-induced PDS was significantly reduced or abolished in Ringer's containing aminophosphonovalerate. Cells displaying the responses described were labeled with neurobiotin. Those labeled are medium-sized multipolar cells. Their dendrites are usually spiny and can extend superficially up to the cortical surface. Their thin axons give rise to collaterals that branch profusely within the cortex. The main axons project laterally along the circumference of the IC or medially into the commissure separating the collicular hemispheres.