Abstract
Tinnitus, the perception of sound in the absence of external acoustic stimulation, is a common and devastating pathology. It is often a consequence of acoustic trauma or drug toxicity. The neuronal mechanisms of tinnitus are neither yet fully understood nor are effective treatments available. Using a novel behavioral paradigm for measuring tinnitus in the rat based on tone-guided navigation, we show here that the development of long-term noise-induced tinnitus, the most prevalent and clinically important form of human tinnitus, can be abated by local administration of the NMDA antagonist “ifenprodil” into the cochlea in the first 4 days following the noise insult but not afterwards. This suggests that long-term tinnitus undergoes a consolidation-like process, resembling the ontogeny of items in long-term memory. Furthermore, this finding paves the way to potential therapeutic strategies for the prevention of chronic tinnitus once the noise insult had taken place.
Highlights
Tinnitus, the perception of sound in the absence of external acoustic stimulation, is a widespread pathology and affects around 10% of the adult population [1,2,3,4]
We report that the induction of both salicylate-induced and noise-induced tinnitus can be blocked by the local cochlear application of ifenprodil, an antagonist of the 2B subunit of the NMDA receptor (NR2B), a molecule which is implicated in long-term potentiation and behavioral plasticity in the mammalian brain [14,15,16,17,18]
We used a place-tone conditioning paradigm, in which rats learn to associate the presence of a tone with the presence of an escape platform in one of the arms of a water T-maze (WTM), and the absence of that tone with the presence of the escape platform in the opposite arm of the maze
Summary
The perception of sound in the absence of external acoustic stimulation, is a widespread pathology and affects around 10% of the adult population [1,2,3,4]. It is commonly the result of overexposure to noise or overconsumption of drugs such as salicylates. Given the high prevalence and the suffering involved, the neurobiology of tinnitus is of great importance. What is it that alters a perceptual system to experience a phantom percept? Is this a form of runaway plasticity, and can it be blocked? Are its mechanisms shared with those that subserve memory? Evidence has been accumulated to implicate neuroplasticity in tinnitus, including a role for cochlear N-methyl-D-aspartate (NMDA) receptor [7, 11, 12]
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