Abstract
Tinnitus is a common auditory disease worldwide; it is estimated that more than 10% of all individuals experience this hearing disorder during their lifetime. Tinnitus is sometimes accompanied by hearing loss. However, hearing loss is not acquired in some other tinnitus generations. In this study, we injected adult rats with salicylate sodium (SS) (200 mg/kg/day for 10 days) and found no significant hearing threshold changes at 2, 4, 8, 12, 14, 16, 20, or 24 kHz (all p > 0.05). Tinnitus was confirmed in the treated rats via Behaviour Testing of Acoustic Startle Response (ASR) and Gap Prepulse Inhibition Test of Acoustic Startle Reflex (GPIAS). A immunostaining study showed that there is significant loss of anti-CtBP2 puncta (a marker of cochlear inner hair cell (HC) ribbon synapses) in treated animals in apical, middle, and basal turns (all p < 0.05). The ABR wave I amplitudes were significantly reduced at 4, 8, 12, 14, 16, and 20 kHz (all p < 0.05). No significant losses of outer HCs, inner HCs, or HC cilia were observed (all p > 0.05). Thus, our study suggests that loss of cochlear inner HC ribbon synapse after SS exposure is a contributor to the development of tinnitus without changing hearing threshold.
Highlights
Tinnitus is becoming a serious health problem worldwide [1,2,3]
An alternative animal study showed that the mice exposed to noise develop temporary threshold shift (TTS) [14] and irreversible loss of cochlear ribbon synapses that connect cochlear inner HCs and spiral ganglion cells (SGCs) [13, 15]
Bauer et al found behavioural evidence indicating that loss of auditory nerve (AN) fibers in rats may associate with tinnitus [16]; there is significant loss of hearing and HCs in rats after noise exposure
Summary
Tinnitus is becoming a serious health problem worldwide [1,2,3]. It was proposed that tinnitus is probably induced by an imbalance between neuronal excitability and inhibition in the auditory circuit [4, 5]. An alternative animal study showed that the mice exposed to noise develop temporary threshold shift (TTS) [14] and irreversible loss of cochlear ribbon synapses that connect cochlear inner HCs and spiral ganglion cells (SGCs) [13, 15] It is unclear whether loss of cochlear ribbon synapses contributes to tinnitus generation in patients with normal audiogram. Bauer et al found behavioural evidence indicating that loss of auditory nerve (AN) fibers in rats may associate with tinnitus [16]; there is significant loss of hearing and HCs in rats after noise exposure This model may be unsuitable for exploring the etiology of tinnitus with normal audiogram. We present the evidence that an appropriate dose of SS exposure can cause tinnitus with normal audiogram and cochlear HCs, but loss of cochlear ribbon synapse suggesting loss of cochlear inner HC ribbon synapse may largely contribute to SS-induced tinnitus
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