Efferent regulation of hair cells in the turtle cochlea

1982 ◽  
Vol 216 (1204) ◽  
pp. 377-384 ◽  
Keyword(s):  
Membrane Potential ◽  
Hair Cell ◽  
Hair Cells ◽  
Auditory Nerve ◽  
Characteristic Frequency ◽  
Receptor Potential ◽  
Combined Effects ◽  
Intracellular Recordings ◽  
Threshold Elevation ◽  
Nerve Fibres

Intracellular recordings were made from hair cells in the isolated cochlea of the turtle to characterize the inhibition achieved by the cochlea’s efferent innervation. A short train of shocks delivered to the efferent axons produced in the hair cells slow hyperpolarizing synaptic potentials which could be reversed by shifting the membrane potential more negative than about - 80 mV. Throughout the efferent hyperpolarization, there was a reduction of up to 25-fold in the amplitude of the receptor potential for tones presented at the hair cell’s characteristic frequency. Efferent stimulation also was shown to degrade the cell’s tuning properties.It is argued that the combined effects of the hyperpolarization and the loss in hair cell sensitivity could account for a threshold elevation of at least 70 dB in the auditory nerve fibres.

scholarly journals Good vibrations: Music and the single hair cell

2002 ◽  
Vol 24 (6) ◽  
pp. 12-14
Author(s):  
Corné Kros
Keyword(s):  
Hair Cell ◽  
Inner Ear ◽  
Hair Cells ◽  
Auditory Nerve ◽  
Sound Stimulus ◽  
Mechanical Stimuli ◽  
Sensory Receptors ◽  
Nerve Fibres ◽  
Sound Processing ◽  
The Brain

Hair cells are the sensory receptors in the inner ear, and the hair bundles that protrude from their upper surfaces transduce mechanical stimuli into electrical responses. This article examines the key molecules involved in the different stages of sound processing within these extraordinarily sensitive and intricate cells, from the reception of the sound stimulus to the release of neurotransmitters on to the auditory nerve fibres that signal to the brain that a sound has been received.

scholarly journals Noise-induced and age-related hearing loss:  new perspectives and potential therapies

F1000Research ◽  
2017 ◽  
Vol 6 ◽  
pp. 927 ◽  
Author(s):  
M Charles Liberman
Keyword(s):  
Hearing Loss ◽  
Hair Cell ◽  
Sensorineural Hearing Loss ◽  
Hair Cells ◽  
Auditory Nerve ◽  
Cell Loss ◽  
Sensorineural Hearing ◽  
Hair Cell Loss ◽  
Age Related ◽  
Age Related Hearing Loss

The classic view of sensorineural hearing loss has been that the primary damage targets are hair cells and that auditory nerve loss is typically secondary to hair cell degeneration. Recent work has challenged that view. In noise-induced hearing loss, exposures causing only reversible threshold shifts (and no hair cell loss) nevertheless cause permanent loss of >50% of the synaptic connections between hair cells and the auditory nerve. Similarly, in age-related hearing loss, degeneration of cochlear synapses precedes both hair cell loss and threshold elevation. This primary neural degeneration has remained a “hidden hearing loss” for two reasons: 1) the neuronal cell bodies survive for years despite loss of synaptic connection with hair cells, and 2) the degeneration is selective for auditory nerve fibers with high thresholds. Although not required for threshold detection when quiet, these high-threshold fibers are critical for hearing in noisy environments. Research suggests that primary neural degeneration is an important contributor to the perceptual handicap in sensorineural hearing loss, and it may be key to the generation of tinnitus and other associated perceptual anomalies. In cases where the hair cells survive, neurotrophin therapies can elicit neurite outgrowth from surviving auditory neurons and re-establishment of their peripheral synapses; thus, treatments may be on the horizon.

scholarly journals Resolution of subcomponents of synaptic release from post-synaptic currents in rat hair-cell/auditory-nerve fiber synapses

2020 ◽  
Author(s):  
Eric D. Young ◽  
Jingjing Sherry Wu ◽  
Mamiko Niwa ◽  
Elisabeth Glowatzki
Keyword(s):  
Hair Cell ◽  
Nerve Fiber ◽  
Hair Cells ◽  
Auditory Nerve ◽  
Neurotransmitter Release ◽  
Auditory Nerve Fiber ◽  
Vesicle Release ◽  
Synaptic Currents ◽  
Synaptic Release

AbstractThe synapse between inner hair cells and auditory nerve fiber dendrites shows large EPSCs, which are either monophasic or multiphasic. Multiquantal or uniquantal flickering release have been proposed to underlie the unusual multiphasic waveforms. Here the nature of multiphasic waveforms is analyzed using EPSCs recorded in vitro in rat afferent dendrites. Spontaneous EPSCs were deconvolved into a sum of presumed release events with monophasic EPSC waveforms. Results include: first, the charge of EPSCs is about the same for multiphasic versus monophasic EPSCs. Second, EPSC amplitudes decline with the number of release events per EPSC. Third, there is no evidence of a mini-EPSC. Most results can be accounted for by versions of either uniquantal or multiquantal release. However, serial neurotransmitter release in multiphasic EPSCs shows properties that are not fully explained by either model, especially that the amplitudes of individual release events is established at the beginning of a multiphasic EPSC, constraining possible models of vesicle release.

scholarly journals Synaptic migration and reorganization after noise exposure suggests regeneration in a mature mammalian cochlea

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Tyler T. Hickman ◽  
Ken Hashimoto ◽  
Leslie D. Liberman ◽  
M. Charles Liberman
Keyword(s):  
Hair Cell ◽  
Hair Cells ◽  
Auditory Nerve ◽  
Guinea Pigs ◽  
Noise Exposure ◽  
Recovery Period ◽  
Nerve Fibers ◽  
Neural Regeneration ◽  
Adult Mice ◽  
Synaptic Markers

AbstractOverexposure to intense noise can destroy the synapses between auditory nerve fibers and their hair cell targets without destroying the hair cells themselves. In adult mice, this synaptopathy is immediate and largely irreversible, whereas, in guinea pigs, counts of immunostained synaptic puncta can recover with increasing post-exposure survival. Here, we asked whether this recovery simply reflects changes in synaptic immunostaining, or whether there is actual retraction and extension of neurites and/or synaptogenesis. Analysis of the numbers, sizes and spatial distribution of pre- and post-synaptic markers on cochlear inner hair cells, in guinea pigs surviving from 1 day to 6 months after a synaptopathic exposure, shows dramatic synaptic re-organization during the recovery period in which synapse counts recover from 16 to 91% of normal in the most affected regions. Synaptic puncta move all over the hair cell membrane during recovery, translocating far from their normal positions at the basolateral pole, and auditory-nerve terminals extend towards the hair cell’s apical end to re-establish contact with them. These observations provide stronger evidence for spontaneous neural regeneration in a mature mammalian cochlea than can be inferred from synaptic counts alone.

The coding of sound pressure and frequency in cochlear hair cells of the terrapin

1978 ◽  
Vol 203 (1151) ◽  
pp. 209-218 ◽  
Keyword(s):  
Hair Cell ◽  
Hair Cells ◽  
Characteristic Frequency ◽  
Voltage Response ◽  
Recording Electrode ◽  
Small Current ◽  
Cochlear Hair Cells ◽  
Damped Oscillations ◽  
Current Steps ◽  
Two Stages

Intracellular recordings have been made from single hair cells in the cochlea of the terrapin, and the site of recording has been verified by injection of a fluorescent dye through the recording electrode. A hair cell gives periodic voltage responses graded with the intensity and frequency of the sound stimulus, and produces the largest response at its characteristic frequency. When small current steps are injected through the recording electrode, the voltage response of the cell exhibits damped oscillations at its characteristic frequency. The results are consistent with the idea that the cochlear frequency selectivity arises in two stages and it is suggested that the second stage resides within the hair cell itself.

scholarly journals Intersensory Interactions in Hermissenda

1973 ◽  
Vol 62 (2) ◽  
pp. 185-202 ◽  
Author(s):  
Daniel L. Alkon
Keyword(s):  
Hair Cell ◽  
Hair Cells ◽  
Visual Information ◽  
Visual Pathway ◽  
Photic Stimulation ◽  
Intracellular Recordings ◽  
Cell Responses

Hair cells of the Hermissenda statocyst respond to photic stimulation. This response requires the presence of at least one of the two eyes. Two principal hair cell responses to light were observed. The activity of photoreceptors in response to a light step is interrupted during firing of contralateral hair cells. The intersensory interactions between the statocyst and visual pathway underlying these responses were examined with simultaneous intracellular recordings. Evidence is presented that the statocyst of Hermissenda is an important channel for visual information.

Role of L-Type Ca2+ Channels in Transmitter Release From Mammalian Inner Hair Cells I. Gross Sound-Evoked Potentials

1999 ◽  
Vol 82 (6) ◽  
pp. 3307-3315 ◽  
Author(s):  
Si Yi Zhang ◽  
Donald Robertson ◽  
Graeme Yates ◽  
Alan Everett
Keyword(s):  
Hair Cell ◽  
Hair Cells ◽  
Transmitter Release ◽  
Receptor Potential ◽  
Large Change ◽  
Outer Hair Cells ◽  
Generation Process ◽  
Output Stage ◽  
Inner Hair Cells ◽  
Summating Potential

Intracochlear perfusion and gross potential recording of sound-evoked neural and hair cell responses were used to study the site of action of the L-type Ca2+ channel blocker nimodipine in the guinea pig inner ear. In agreement with previous work nimodipine (1–10 μM) caused changes in both the compound auditory nerve action potential (CAP) and the DC component of the hair cell receptor potential (summating potential, or SP) in normal cochleae. For 20-kHz stimulation, the effect of nimodipine on the CAP threshold was markedly greater than the effect on the threshold of the negative SP. This latter result was consistent with a dominant action of nimodipine at the final output stage of cochlear transduction: either the release of transmitter from inner hair cells (IHCs) or the postsynaptic spike generation process. In animals in which the outer hair cells (OHCs) had been destroyed by prior administration of kanamycin, nimodipine still caused a large change in the 20-kHz CAP threshold, but even less change was observed in the negative SP threshold than in normal cochleae. When any neural contamination of the SP recording in kanamycin-treated animals was removed by prior intracochlear perfusion with TTX, nimodipine caused no significant change in SP threshold. Some features of the data also suggest a separate involvement of nimodipine-sensitive channels in OHC function. Perfusion of the cochlea with solutions containing Ni2+ (100 μM) caused no measurable change in either CAP or SP. These results are consistent with, but do not prove, the notion that L-type channels are directly involved in controlling transmitter release from the IHCs and that T-type Ca2+channels are not involved at any stage of cochlear transduction.

scholarly journals Hair Cell Interactions in the Statocyst of Hermissenda

1973 ◽  
Vol 62 (5) ◽  
pp. 618-642 ◽  
Author(s):  
Peter B. Detwiler ◽  
Daniel L. Alkon
Keyword(s):  
Hair Cell ◽  
Mechanical Stimulation ◽  
Hair Cells ◽  
Spike Activity ◽  
Synaptic Potential ◽  
Intracellular Recordings ◽  
Electrical Synapses ◽  
Generator Potential ◽  
Inhibitory Interactions ◽  
The Brain

Hair cells in the statocyst of Hermissenda crassicornis respond to mechanical stimulation with a short latency (<2 ms) depolarizing generator potential that is followed by hyperpolarization and inhibition of spike activity. Mechanically evoked hyperpolarization and spike inhibition were abolished by cutting the static nerve, repetitive mechanical stimulation, tetrodotoxin (TTX), and Co++. Since none of these procedures markedly altered the generator potential it was concluded that the hyperpolarization is an inhibitory synaptic potential and not a component of the mechanotransduction process. Intracellular recordings from pairs of hair cells in the same statocyst and in statocysts on opposite sides of the brain revealed that hair cells are connected by chemical and/or electrical synapses. All chemical interactions were inhibitory. Hyperpolarization and spike inhibition result from inhibitory interactions between hair cells in the same and in opposite statocysts.

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