An Exploratory Study of Bimodal Electro-Aural Stimulation Through the Ear Canals for Tinnitus.

Objective: The aim of this study was to explore the potential for bimodal auditory and noninvasive electrical stimulation at the ears to alleviate tonal, somatic tinnitus that was investigated in a small preliminary trial (11 participants).

Design: Auditory stimulation took the form of short "notched noise" bursts customized to each participant's tinnitus percept. Simultaneous pulsed electrical stimulation, intended to facilitate neuroplasticity, was delivered via hydrogel electrodes placed in opposite ears.

Noise-induced cochlear neuropathy is selective for fibers with low spontaneous rates.

Acoustic overexposure can cause a permanent loss of auditory nerve fibers without destroying cochlear sensory cells, despite complete recovery of cochlear thresholds (Kujawa and Liberman 2009), as measured by gross neural potentials such as the auditory brainstem response (ABR). To address this nominal paradox, we recorded responses from single auditory nerve fibers in guinea pigs exposed to this type of neuropathic noise (4- to 8-kHz octave band at 106 dB SPL for 2 h). Two weeks postexposure, ABR thresholds had recovered to normal, while suprathreshold ABR amplitudes were reduced.

Primary neural degeneration in the Guinea pig cochlea after reversible noise-induced threshold shift.

Recent work in mouse showed that acoustic overexposure can produce a rapid and irreversible loss of cochlear nerve peripheral terminals on inner hair cells (IHCs) and a slow degeneration of spiral ganglion cells, despite full recovery of cochlear thresholds and no loss of inner or outer hair cells (Kujawa and Liberman, J Neurosci 29:14077-14085, 2009). This contrasts with earlier ultrastructural work in guinea pig suggesting that acute noise-induced neural degeneration is followed by full regeneration of cochlear nerve terminals in the IHC area (Puel et al., Neuroreport 9:2109-2114, 1998; Pujol and Puel, Ann N Y Acad Sci 884:249-254, 1999).

Adaptation reduces spike-count reliability, but not spike-timing precision, of auditory nerve responses.

Sensory systems use adaptive coding mechanisms to filter redundant information from the environment to efficiently represent the external world. One such mechanism found in most sensory neurons is rate adaptation, defined as a reduction in firing rate in response to a constant stimulus. In auditory nerve, this form of adaptation is likely mediated by exhaustion of release-ready synaptic vesicles in the cochlear hair cell.

The effects of intense sound exposure on phase locking in the chick (Gallus domesticus) cochlear nerve.

Little is known about changes that occur to phase locking in the auditory nerve following exposure to intense and damaging levels of sound. The present study evaluated synchronization in the discharge patterns of cochlear nerve units collected from two groups of young chicks (Gallus domesticus), one shortly after removal from an exposure to a 120-dB, 900-Hz pure tone for 48 h and the other from a group of non-exposed control animals. Spontaneous activity, the characteristic frequency (CF), CF threshold and a phase-locked peri-stimulus time histogram were obtained for every unit in each group.

Evidence that rapid vesicle replenishment of the synaptic ribbon mediates recovery from short-term adaptation at the hair cell afferent synapse.

We have employed both in vitro patch clamp recordings of hair cell synaptic vesicle fusion and in vivo single unit recording of cochlear nerve activity to study, at the same synapse, the time course, control, and physiological significance of readily releasable pool dynamics. Exocytosis of the readily releasable pool was fast, saturating in less than 50 ms, and recovery was also rapid, regaining 95% of its initial amplitude following a 200-ms period of repolarization. Longer depolarizations (greater than 250 ms) yielded a second, slower kinetic component of exocytosis.