Electrical stimulation may decrease cell death or promote sprouting to accelerate early recovery. Testosterone may affect the actual rate of axonal regeneration and produce acceleration in functional recovery. By targeting different stages of neural regeneration, the synergy of electrical stimulation and testosterone appears to have promise as a neurotherapeutic strategy for facial nerve injury.

Six chinchillas (12 ears) were equally divided into three groups: Two groups received six hours of noise exposure (NEϭ octave band, 105 dB SPL, centered at 4 kHz) and treated with either saline or CARBA (5.2mg/kg). One group received no noise and no treatment (controls). Treatments were given IP, one hour before and after noise and BID for two days prior to NE. Animals were humanely euthanized at two hours post-NE. Cochleae were processed for microscopy. Four IHCs from the basal turn of each ear, 16 IHCs from each group, were examined for synaptic edema using imaging software. RESULTS: Synaptic edema was found in 16 of 16 IHCs (100%) in the noise-saline, 4 of 16 (25%) in the noise-CARBA (pϽ0.01), and 2 of 16 in the controls (12.5%) (pϽ0.01). The number of dendrite edematous spaces per IHC ranged from 3-10 (average 4.13) in the noise-saline, from 1-6 (average 3) in the noise-CARBA, and from 1-4 (average 2.5) in the controls. Edema area was 34.52Ϯ21.27 (meanϮSD) in the noise-saline, 5.43Ϯ3.69 in the noise-CARBA (pϽ0.001), and 6.61Ϯ6.51 in the controls (pϽ0.003). CONCLUSION: The findings suggested that afferent dendrite edema from acoustic overexposure was prevented by a glutamate NMDA receptor antagonist carbamathione in a chinchilla model. SIGNIFICANCE: Using glutamate NMDA receptor antagonists for prevention of synaptic edema in acoustic overexposure will allow development of therapies to treat NIHL.