Abstract
Hearing loss often results in plastic changes in the central auditory pathways, which may be involved in the generation of tinnitus, a phantom auditory sensation. However, although animal studies have consistently shown increased neural activity in auditory structures after hearing loss, tinnitus does not always develop. It has therefore been suggested that non-auditory structures perform a gating or regulatory role that determines whether the increased activity in auditory structures leads to conscious perception. Recent evidence points to the paraflocculus of the cerebellum as having such a role. Therefore, we investigated the early effects of hearing loss on gene expression in guinea pig paraflocculus. Gene expression was investigated after two weeks recovery from either acoustic or mechanical cochlear trauma. The genes investigated in our study were associated with inhibitory neurotransmission (GABA-A receptor subunit alpha 1; glutamate decarboxylase 1), excitatory neurotransmission (glutamate receptor NMDA subunit 1), and regulation of transmitter release (member of RAB family of small GTPase). Our results show increased mRNA levels of glutamate decarboxylase 1 in ipsilateral paraflocculus with no difference between the different methods of cochlear trauma. Early modulation of gene expression in the paraflocculus suggests that an early effect of hearing loss may affect the influence of this structure on auditory processing.
Highlights
It is well known that trauma to the cochlea results in a reduced sensitivity to sound[1,2], and leads to a variety of physiological changes in the central nervous system
Central neural changes following hearing loss have been described using many different animal models and include changes in tonotopic maps[3,4], increased synchronous firing patterns[5,6,7] and increased spontaneous firing rates[6,7,8,9,10,11]. This abnormal neural activity observed in the central auditory pathways following cochlear trauma has been suggested to play a role in the development of tinnitus, a phantom auditory sensation that is often associated with the presence of hearing loss[12,13,14]
A trauma to the peripheral auditory receptor could serve as a trigger for the abnormal changes seen in the central auditory pathways, other brain regions are likely to be involved in giving rise to the eventual phantom auditory perception
Summary
It is well known that trauma to the cochlea results in a reduced sensitivity to sound[1,2], and leads to a variety of physiological changes in the central nervous system. Central neural changes following hearing loss have been described using many different animal models and include changes in tonotopic maps[3,4], increased synchronous firing patterns[5,6,7] and increased spontaneous firing rates[6,7,8,9,10,11] This abnormal neural activity observed in the central auditory pathways following cochlear trauma has been suggested to play a role in the development of tinnitus, a phantom auditory sensation that is often associated with the presence of hearing loss[12,13,14]. Ablation of the paraflocculus in rats before the induction of tinnitus results in the prevention or reduction of subsequent tinnitus[17]
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