Single-neuron labeling and chronic cochlear pathology. II. Stereocilia damage and alterations of spontaneous discharge rates

Liberman, M. Charles; Dodds, Leslie W.

doi:10.1016/0378-5955(84)90024-8

Cited by 219 publications

(111 citation statements)

References 17 publications

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“…Indeed, loss or damage of stereocilia might induce a hyperpolarization of inner hair cells. This, in turn, decreases spontaneous firing rate through a decrease in spontaneous release of neurotransmitter (Liberman and Dodds, 1984). This localized decrease in firing rate could thereafter induce a cascade of central changes leading to tonotopic map reorganization .…”

Section: Discussionmentioning

confidence: 99%

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Enriched Acoustic Environment after Noise Trauma Reduces Hearing Loss and Prevents Cortical Map Reorganization

Noreña¹,

Eggermont²

2005

J. Neurosci.

297

188

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Exposure to sound of sufficient duration and level causes permanent damage to the peripheral auditory system, which results in the reorganization of the cortical tonotopic map. The changes are such that neurons with pre-exposure tuning to frequencies in the hearing loss range now become tuned to frequencies near the near-normal lower boundary of the hearing loss range, which thus becomes over represented. However, cats exposed to a traumatizing noise and immediately thereafter placed for a few weeks in an enriched acoustic environment presented a much-restricted hearing loss compared with similarly exposed cats that were placed for the same time in a quiet environment. The enriched environment spectrally matched the expected hearing loss range and was ϳ40 dB above the level of the expected hearing loss. The hearing loss in the quiet environment-reared cats ranged from 6 to 32 kHz with the largest loss (on average, 40 dB) ranging from 24 to 32 kHz. In contrast, the hearing loss in the enriched-environment cats was restricted to 6 -8 kHz at a level of, on average, 35 dB and with 16 -32 kHz having normal thresholds. Despite the remaining hearing loss for the enriched-environment cats in the 6 -8 kHz range, plastic tonotopic map changes in primary auditory cortex could no longer be demonstrated, suggesting that the enriched acoustic environment prevents this reorganization. This finding has implications for the treatment of hearing disorders, such as tinnitus, that have been linked to cortical tonotopic map reorganization.

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Section: Discussionmentioning

confidence: 99%

“…The reduction in spontaneous and driven firing rate after hearing impairment may be induced by damage to inner hair cell stereocilia (Liberman and Dodds, 1984). Indeed, loss or damage of stereocilia might induce a hyperpolarization of inner hair cells.…”

Section: Discussionmentioning

confidence: 99%

Enriched Acoustic Environment after Noise Trauma Reduces Hearing Loss and Prevents Cortical Map Reorganization

Noreña¹,

Eggermont²

2005

J. Neurosci.

297

188

View full text Add to dashboard Cite

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“…In the periphery, acoustic injury typically results in reduced sound-evoked and spontaneous activity in the cochlear nerve (Heinz and Young 2004;Liberman and Dodds 1984a;Liberman and Kiang 1984). This overall reduction in peripheral neural activity occurs both because damage to (or loss of) the sensory cells reduces (or eliminates) synaptic transmission to cochlear nerve terminals (Liberman and Dodds 1984b;Liberman and Kiang 1978) and because overdriving the cochlear neurons during exposure induces glutamate excitotoxicity that destroys their peripheral terminals and leads to widespread cochlear nerve degeneration, even when the hair cells survive (Puel et al 1998;Wang et al 2002).…”

Section: Discussionmentioning

confidence: 99%

Is noise-induced cochlear neuropathy key to the generation of hyperacusis or tinnitus?

Hickox

Liberman

2014

Journal of Neurophysiology

291

261

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Here we ask whether this noise-induced primary neuronal degeneration results in abnormal auditory behavior, based on the acoustic startle response (ASR) and prepulse inhibition (PPI) of startle. Responses were measured in mice exposed either to a "neuropathic" noise or to a lower-intensity, "nonneuropathic" noise and in unexposed control mice. Mice with cochlear neuropathy displayed hyperresponsivity to sound, evidenced by enhanced ASR and PPI, while exposed mice without neuronal loss showed controllike responses. Gap PPI tests, often used to assess tinnitus, revealed limited gap detection deficits in mice with cochlear neuropathy only for certain gap-startle latencies, inconsistent with the presence of tinnitus "filling in the gap." Despite significantly reduced wave 1 of the auditory brainstem response, representing cochlear nerve activity, later peaks were unchanged or enhanced, suggesting compensatory neural hyperactivity in the auditory brainstem. Considering the rapid postexposure onset of both cochlear neuropathy and exaggerated startle-based behavior, the results suggest a role for cochlear primary neuronal degeneration, per se, in the central neural excitability that could underlie the generation of hyperacusis. acoustic startle response; prepulse inhibition; auditory brainstem response; noise-induced hearing loss; acoustic trauma

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“…Experimental evidence from activation of the cochlear efferent system (Brown & Nuttall, 1984), the specific lesions produced by ototoxic drug and noise damage (Evans & Harrison, 1976;Liberman & Dodds, 1984) and theoretical models of cochlear mechanics (de Boer, 1983;Neely & Kim, 1986) all suggest that the outer hair cells of the cochlear partition are likely to be the force generators within the cochlea. In support of the idea of an active role for outer hair cells, it is known that hair cells are immunoreactive for a variety of contractile proteins (Flock, 1983) and manipulating the surrounding medium of hair cells produces relatively slow (time scale 10-100 s) alterations in the outer hair cell length.…”

Section: Introductionmentioning

confidence: 99%

A fast motile response in guinea‐pig outer hair cells: the cellular basis of the cochlear amplifier.

Ashmore¹

1987

The Journal of Physiology

801

453

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SUMMARY1. Outer hair cells from the cochlea of the guinea-pig were isolated and their motile properties studied in short-term culture by the whole-cell variant of the patch recording technique.2. Cells elongated and shortened when subjected to voltage steps. Cells from both high-and low-frequency regions of the cochlea responded with an elongation when hyperpolarized and a shortening when depolarized. The longitudinal motion of the cell was measured by a differential photosensor capable of responding to motion frequencies 0-40 kHz.3. Under voltage clamp the length change of the cell was graded with command voltage over a range + 2 ,tm (approximately 4 % ofthe length) for cells from the apical turns of the cochlea. The mean sensitivity of the movement was 2 11 nm/pA injected current, or 19'8 nm/mV membrane polarization. 4. The kinetics of the cell length change during a voltage step were measured. Stimulated at their basal end, cells from the apical (low-frequency) cochlear turns responded with a latency of between 120 and 255 gs. The cells thereafter elongated exponentially by a process which could be characterized by three time constants, one with value 240 ,us, and a second in the range 1-3-2-8 ms. A third time constant with a value 20-40 ms characterized a slower component which may represent osmotic changes.5. Consistent with the linearity shown to voltage steps, sinusoidal stimulation of the cell generated movements which could be measured at frequencies above 1 kHz. The phase of the movement relative to the stimulus continued to grow with frequency, suggesting the presence of an absolute delay in the response of about 200 gs.6. The electrically stimulated movements were insensitive to the ionic composition of the cell, manipulated by dialysis from the patch pipette. The responses occurred when the major cation was K+ or Na+ in the pipette. Loading the cell with ATPfree solutions or calcium buffers did not inhibit the response.7. It is concluded that interaction between actin and myosin, although present in the cell, is unlikely to account for the cell motility. Instead, it is proposed that outer hair cell motility is associated with structures in the cell cortex. The implications for cochlear mechanics of such force generation in outer hair cells are discussed. 11-2

show abstract

Single-neuron labeling and chronic cochlear pathology. II. Stereocilia damage and alterations of spontaneous discharge rates

Cited by 219 publications

References 17 publications

Enriched Acoustic Environment after Noise Trauma Reduces Hearing Loss and Prevents Cortical Map Reorganization

Enriched Acoustic Environment after Noise Trauma Reduces Hearing Loss and Prevents Cortical Map Reorganization

Is noise-induced cochlear neuropathy key to the generation of hyperacusis or tinnitus?

A fast motile response in guinea‐pig outer hair cells: the cellular basis of the cochlear amplifier.

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