Progressive centralization of midbrain hyperactivity after acoustic trauma

Partial hearing loss is known to cause increased spontaneous activity at several stages of the central auditory pathways, and this phenomenon has been suggested as a possible neural substrate for tinnitus, a phantom hearing sensation. One recent study in guinea pig has suggested that approximately 6 weeks after acoustic trauma, the increased spontaneous activity in inferior colliculus is not intrinsically generated in the central nucleus but is dependent on afferent input from the cochlea. This was unexpected in view of the fact that tinnitus in human patients can persist after severing of the auditory nerve. In this study, we show that when recovery time after acoustic trauma is extended to 8 and 12 weeks, cochlear ablation does not significantly decrease the increased spontaneous activity measured in the inferior colliculus. This result demonstrates for the first time that central hyperactivity that develops after acoustic trauma transitions from an early stage when it is dependent on continued peripheral afferent input to a later stage in which the hyperactivity is intrinsically generated within the central nervous system.