Many investigations have shown that modulation of sensory input, either by over stimulation or sensory deprivation, can cause a reorganization of structures located high in the central nervous system (CNS). Although most of these studies had focused on studying changes in the function and tonotopic organization of the sensory cortex, recent evidence has suggested that plastic changes in specific subcortical nuclei of sensory systems may also occur in response to modulation of sensory input, and may be partially responsible for changes reflected at the level of the cortex. In the present study we investigated the effects of noise exposure (4-kHz continuous tone at 104 dB sound pressure level (SPL) for 30 min duration) on the processing of auditory information at the level of the inferior colliculus (IC). We studied how evoked potentials recorded from the surface of the IC changed as a function of the duration of the tone bursts used as stimuli. We measured the amplitude of a peak that is generated postsynaptically in the IC in response to tone bursts between 1 and 6 ms duration. In animals that were not exposed to the tone, the amplitude of this peak decreased with increasing stimulus duration, but after tone exposure, the decrease in the amplitude of this peak was significantly less than in the animals not exposed to the tone. A microinjection of the GABAA antagonist, bicucullene, into the IC in the animals not exposed to the tone caused the amplitude of the peak to be less dependent on tone burst duration, which indicates that the decrease in the amplitude of this component of the response from the IC with increasing stimulus duration is a result of GABAA mediated inhibition on IC neurons. The tone exposure caused a similar decrease in amplitude of this component of the response from the IC, thus indicating that noise exposure reduced the GABAA mediated component of this function. This is supported by the finding that microinjections of bicucullene into the IC of noise-exposed animals did not significantly change the relationship between the amplitude of this peak and the stimulus duration.