Influence of the paraflocculus on normal and abnormal spontaneous firing rates in the inferior colliculus.

Spontaneous firing rates of neurons in the central auditory pathway, such as in the inferior colliculus, are known to be increased after cochlear trauma. This so-called hyperactivity is thought to be involved in the generation of tinnitus, a phantom auditory perception. Recent research in an animal model suggests behavioural signs of tinnitus can be significantly reduced by silencing or removal of the paraflocculus (PF) of the cerebellum. The current study investigated the effects of acute PF removal on spontaneous firing rates recorded from single neurons in the right inferior colliculus of guinea pigs with normal hearing (which did not receive acoustic trauma) or with hearing loss caused by acoustic trauma. Spontaneous firing rates were obtained at either 2 or 13 weeks after initial surgery on the left side. In half of the animals in each group the left PF was removed immediately prior to the spontaneous firing rates recordings. In the acoustic trauma groups, spontaneous firing rates in the inferior colliculus were higher when the PF was removed compared to animals with an intact PF. This effect of PF removal was not observed in animals that did not receive acoustic trauma. These results suggest that the PF has a tonic inhibitory effect on hyperactivity in the inferior colliculus in animals with hearing loss, but not on normal spontaneous firing rates in normal hearing animals.

Spontaneous hyperactivity in the auditory midbrain: relationship to afferent input.

Hyperactivity in the form of increased spontaneous firing rates of single neurons develops in the guinea pig inferior colliculus (IC) after unilateral loud sound exposures that result in behavioural signs of tinnitus. The hyperactivity is found in those parts of the topographic frequency map in the IC where neurons possess characteristic frequencies (CFs) closely related to the region in the cochlea where lasting sensitivity changes occur as a result of the loud sound exposure. The observed hyperactivity could be endogenous to the IC, or it could be driven by hyperactivity at lower stages of the auditory pathway. In addition to the dorsal cochlear nucleus (DCN) hyperactivity reported by others, specific cell types in the ventral cochlear nucleus (VCN) also show hyperactivity in this animal model suggesting that increased drive from several regions of the lower brainstem could contribute to the observed hyperactivity in the midbrain. In addition, spontaneous afferent drive from the cochlea itself is necessary for the maintenance of hyperactivity up to about 8 weeks post cochlear trauma. After 8 weeks however, IC hyperactivity becomes less dependent on cochlear input, suggesting that central neurons transition from a state of hyperexcitability to a state in which they generate their own endogenous firing. The results suggest that there might be a "therapeutic window" for early-onset tinnitus, using treatments that reduce cochlear afferent firing.