Glutamate released from the efferent synapses left side activates group I mGluRs on presynaptic efferent terminals and enhances ACh release and efferent synaptic inhibition to the IHC. During the developmental critical period immature IHCs fire action potentials and release glutamate into the synaptic cleft. In fact, activation of group I metabotropic glutamate receptors mGluR1s enhances ACh release, most likely through the activation p.
The longitudinal distribution of GABAergic terminals beneath OHCs varies from species to species: apical half in guinea pigs and throughout the cochlea in mouse. The function of the GABAergic innervation to hair cells and the exact molecular targets are poorly understood. Therefore, a presynaptic site of action for GABA is expected. In summary, tight control of ACh release from efferent terminals is exerted through the presence of presynaptic neurotransmitter receptors, namely GABA B Wedemeyer et al.
In brief, whereas GABA inhibits, glutamate enhances ACh release, providing a negative and positive feedback to efferent inhibition, respectively. GABA most likely has a neuronal efferent origin, whereas glutamate is a spillover from the nearby IHC endogenous release of glutamate. This tight regulation of ACh release at MOC terminals might act in concert with the short-term synaptic plasticity phenomena known to shape the strength of cochlear inhibition.
A common property of most synapses is that they can keep track of their previous activity by means of synaptic plasticity. Each synapse can integrate several forms of plasticity leading to changes in synaptic strength and this plays a critical role in information transfer and neural processing.
Thus, synaptic strength can be reduced for hundreds of milliseconds to seconds leading to depression, or it can be enhanced during hundreds of milliseconds to seconds resulting in facilitation. The correct operation of this feedback requires a careful match between the acoustic stimulus and the strength of cochlear inhibition. A low probability of release at rest, and facilitation of responses at high frequency stimulation, is a common feature of efferent synapses Art et al. The first reports of short-term synaptic plasticity in efferent terminals were described in turtle hair cells, where the resting probability of release at the hair cell efferent synapse was low, ranging from 0.
Thus, single shocks to the efferents generated hair cell membrane hyperpolarization with an average amplitude of less than 1 mV. The p. Similar results have been found in rat P7—11 IHCs. With repeated stimulation, IPSCs are both larger and more prolonged, likely due to facilitation and summation. Facilitation combined with postsynaptic summation significantly increase the reliability and strength of synaptic transmission during repetitive efferent activity Ballestero et al. The overlap between spontaneous and evoked IPSCs amplitude histograms has led to the proposal that, on average, one vesicle is released upon arrival of an action potential to the MOC—OHC efferent terminal.
The observation that in mice, OHCs from the apical region where recordings were performed are usually innervated by one efferent fiber Maison et al. However, shortage of synaptic vesicles cannot account for the low resting probability of release since efferent terminals have large numbers of vesicles Fuchs et al. The implication of this result is that the efferent terminal is prepared to recruit synaptic vesicles when stimulation is repetitive and at sufficiently high frequencies so that facilitation of transmitter release can occur. The unreliability of transmitter release at the MOC—OHC synapse at low frequency stimulation has been attributed to the stochastic nature of release, rather than to axonal threshold variations or conduction failures Ballestero et al.
The negative feedback loop provided by the coupling between L-type voltage-gated calcium channels and BK channels Zorrilla de San Martin et al. Thus, as reported by Ballestero et al synaptic events occur sparsely at 10 Hz but increase in frequency and amplitude of individual responses as stimulation frequency increases Figure 3. As expected, a sustained and enhanced hyperpolarization of the OHCs is observed in response to high-frequency MOC stimulation Figure 3.
The strengthening of synaptic transmission at high frequency stimulation of MOC terminals is accounted for by both facilitation and summation of OHCs synaptic responses. Ballestero et al. Since the increase in the postsynaptic response during repetitive stimulation correlates with an increase in the probability of release and not with an increase in the mean amplitude of IPSCs, facilitation is due to a presynaptic p.
Facilitation of efferent transmitter release. Facilitation of transmitter release contributes to the increase in the postsynaptic response during high-frequency stimulation. Responses to 10 shock trains gray traces were applied at different frequencies A—E. The black trace is the average response of repetitions at each frequency. Reproduced from Ballestero et al. Hyperpolarization in response to efferent stimulation.
The black trace is the average response obtained upon repetitions of the train. This would allow the MOC efferent feedback to operate in a kind of failsafe mode. Thus, OHCs would ignore spontaneous or inadvertent activity and only respond when efferents are strongly stimulated. Summation of efferent responses. Summation contributes to the increment of the postsynaptic response during high-frequency stimulation. Simulated responses were derived from a response A, inset considering only temporal summation gray traces or facilitation by taking into account the change in the probability of release black traces for every shock.
Simulation plots of normalized current versus pulse number were constructed considering only summation B or summation and facilitation C. D: Experimental plot of normalized current versus pulse number. Summation and facilitation best fit the experimental data. E—H: Representative traces of the simulated single sweep responses.
Nearly all vertebrate hair-cell sense organs have an efferent innervation. The most ancient efferents synapsed on a p. This hypothesis is further based on the fact that after ear ablation developing efferents join the facial motor neurons, most likely reverting to their ancestral condition Fritzsch, Moreover, inner ear efferent neurons and motor neurons share a common embryological origin Fritzsch, For an extended review of the development of the efferent system see Simmons, MOC neurons rely on high-frequency trains rather than single shocks to inhibit auditory function, and the strength of the efferent effect increases as the frequency of stimulation increases.
Left-axis: Efferent effect quantified as the ratio between the amplitude of the N1 component of the compound action potential. Right-axis: Increase in sound intensity threshold shift in decibels necessary to evoke an afferent discharge as a function of the efferent stimulation frequency. Efferent axons innervate the mouse cochlea as early as embryonic day 13 Bruce et al.
The molecular cues that guide efferent axons to the inner ear are not well understood. Reconstructions of the efferent innervation in hamsters has shown that anterograde biocytin and horseradish peroxidase labeled efferent axons terminate on or below IHCs prior to P5. At the electron microscopy level, small labeled terminals containing densely packed synaptic vesicles are observed both adjacent to IHCs axosomatic as well as apposed to afferent and efferent fibers below IHCs prior to P5. Similar results have been obtained in rats and cats Bruce et al. Competition of afferent and efferent terminals for synaptic space below OHCs might explain the coincidence of efferent arrival and the decrease of afferent terminals on OHC Pujol, Moreover, IHCs of wild-type mice lack responses after the onset of hearing Katz et al.
This is accompanied by SK-coupled ACh responses and the first evidence of synaptic currents. Moreover, IHC with efferent synaptic activity are only seen when the SK current is present, suggesting that SK2 expression is correlated with functional synapses Roux et al. Although not tested, proteins known to form a macromolecular complex with SK2 channels, such as calmodulin, protein kinase CK2, and protein phosphatase 2A Bildl et al. Given the sign reversal when nAChRs are coupled to SK channels, one could speculate that SK-mediated hyperpolarization compared to ACh-mediated depolarization might be essential for synaptic maturation.
In addition, SK channels are also important for the maintenance of the synapse, since synaptic currents disappear with the loss of functional SK currents after the onset of hearing Katz et al. In addition, efferent innervation progressively degenerates in SK2 Kong et al. Experiments in isolated OHCs from gerbils and rats suggest that the onset of acetylcholine-induced responses begins on or after P6. This response becomes functionally mature by P12 when coupling to the SK potassium current is always observed.
Therefore, establishing correctly organized and appropriately adjusted synaptic circuits is a crucial event during "critical periods" of brain development, an early postnatal epoch of plasticity during which large-scale changes take place. One key issue discussed in developmental neuroscience is the question of how the specificity of synaptic connections in these networks are established in such a precise manner.
Several major factors are thought to play a crucial role. In general, internal factors i. On the other hand, activity-dependent developmental processes play a key role and are subdivided into those associated with spontaneous activity and those depending on sensory-evoked activity. The auditory system in many mammals is very immature at birth but precisely organized in adults. Consequently, the early steps in the generation of the basic auditory brainstem circuitry are not influenced by acoustically driven activity.
With maturation, a number of changes reduce IHC spiking. These changes trigger the transformation of a developing epithelium with active synaptogenesis to a sensing epithelium, where synaptic contacts have stabilized and mechanical input is transduced into receptor potentials in IHCs in a graded manner. The spontaneous activity in auditory nerve fibers before the onset of hearing is propagated to central auditory nuclei Tritsch et al. Thus, changes in afferent activity are known to lead to changes in synaptic properties in higher brainstem p. The origin of this pre-hearing spontaneous activity is still a matter of debate.
However, Johnson Johnson et al. Although efferent input is not required to initiate this bursting activity Tritsch et al. This preserves the inhibitory signature of the efferent system to ensure normal development of the auditory system. This indicates that the precise temporal pattern of spontaneous prehearing activity is important for the formation of tonotopy in the central auditory pathway and that the transient efferent cholinergic innervation to IHCs is crucial to maintain this temporal pattern.
It is interesting to note that during AMPA-mediated excitotoxicity in the adult guinea pig cochleas, which results in swelling and disappearance of radial afferents below IHCs, vesiculated efferents sometimes with postsynaptic cisterns make transient direct contacts with IHCs Ruel et al. These direct efferent contacts resemble those seen during the critical period of early stages of IHCs synaptogenesis and disappear as efferents make normal axo-dendritic synapses with the regenerated auditory neurites. The re-appearance of efferent contacts below IHCs during damage and aging is intriguing.
If re-appearance of direct efferent contacts in IHCs were to be reported in all these conditions, a re-emergence of a developmental-like critical period could be suggested. Much progress has been made concerning the anatomy, physiology, and molecules involved in the MOC innervation to the inner ear hair cells. Plasticity features of the MOC-hair cell synapse ensure low probability of release at rest and facilitation of responses at high frequency stimulation.
These are important to provide a fine tuning of cochlear amplification, since efferent firing frequency increases linearly with sound intensity. Moreover, the increase of MOC firing rate with sound intensity is consistent with the proposal that the efferent system protects the inner ear from noise-induced trauma. Future studies should provide a deeper insight on the functional roles of MOC activity in audition.
The participation of the efferent innervation during the critical period and the "re-opening" of a critical period-like epoch during cochlear damage should be investigated further as a window for intervention during trauma. Art, J. Efferent regulation of hair cells in the turtle cochlea.
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Short term synaptic plasticity regulates the level of olivocochlear inhibition to auditory hair cells.
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Journal of Neuroscience 32 47 , —a. Facilitating efferent inhibition of inner hair cells in the cochlea of the neonatal rat. Journal of Physiology Pt 1 , 49— Time course and calcium dependence of transmitter release at a single ribbon synapse. Granger, A. Cotransmission of acetylcholine and GABA. Neuropharmacology , 40— Grant, L. Two modes of release shape the postsynaptic response at the inner hair cell ribbon synapse. Journal of Neuroscience 30 12 , — Guinan, J.
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Efferent Innervation to the Cochlea
Channel opening results in bundle relaxation and a displacement of the bundle in the excitatory direction. At the same time, when calcium enters the cell via the transduction channel, fast adaptation occurs, which resets the position of the tip links and generates a negative movement of the bundle. If the bundle is moved further, transduction channels reopen.
Cochlear amplification may also be driven by somatic motility in OHCs via activation of the prestin molecules densely packed along the basolateral membrane. Somatic motility requires prestin, a voltage-sensitive membrane protein that is abundant in the lateral membranes of mammalian OHCs but absent in many non-mammalian vertebrates. The somatic motility theory for cochlear amplification posits that sound stimuli generate receptor potentials that evoke voltage-dependent conformational changes in prestin, such that the protein contracts with depolarization and expands with hyperpolarization.
Because the collective motion of the densely packed molecules occurs parallel to the lateral membranes, OHCs shorten and elongate with changes in membrane potential. Synchronous motion of OHC cell bodies with forces of this amplitude is predicted to amplify the overall motion of the basilar membrane in phase with the sound stimulus. However, because somatic motility depends on the hair cell membrane potential, the membrane time constant likely limits the ability of the receptor potential to follow the sound stimulus; thus, force production may also be limited at high frequencies to which auditory organs are known to be sensitive.
Mechanisms may be present that decrease this time constant, allowing high-frequency operation. In addition, because cochlear amplification also occurs in lower vertebrates that lack OHCs and prestin, a second mechanism has been invoked. An alternative model suggests that the forces generated in the hair bundle are sufficient to drive amplification of sound stimuli in the auditory organs of many different species.
Adaptation is observed during steady deflection of the bundle in the excitatory direction, which causes an initial activation of transduction channels, followed by a decline in the response as transduction channels close Figure 2B. The instantaneous activation curve measured after ms or so is shifted to the right, relative to its position at rest Figure 2B.
Tension on transduction channels relaxes during the deflection so that additional deflection can reactivate the channels. Similarly, a negative deflection that closes channels is followed by adaptation that increases the tension and shifts the activation curve to the left. This process commonly allows hair cells to retain high sensitivity over a broad operating range and filters out slower stimuli in favor of rapid stimuli. Although the mechanism of fast adaptation is controversial, there is agreement that fast adaptation can result in active hair bundle movements. This active process arises at a point in the stimulus-response relation where there is great instability in the system, with a back-and-forth interplay between a transduction channel opening, b relaxation of the hair bundle that results from channel opening, followed by c rebound tension that arises from the adaptation process Figure 2C.
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This phenomena, mathematically identified as a Hopf bifurcation, can contribute to bundle oscillations and may feed energy back into the organ of Corti. To tease apart the relative contributions of somatic motility and hair bundle motility will require selective inactivation in live animals.
However, in mammals, both mechanisms may coexist and cochlear amplification may require both to be functional. Interestingly, while somatic motility has no intrinsic tuning, bundle motility can be tuned by the properties of adaptation. Because mature hair cells lack voltage-gated sodium channels, they do not generate action potentials. Rather, changes in transduction channel activity evoke graded receptor potentials of up to 40 mV. The receptor potential is modified by the activity of voltage- and ion-sensitive conductances in the basolateral membrane.
In some hair cells, depolarizing receptor potentials elicit oscillations of the membrane potential, which may serve to tune the cell to a particular stimulus frequency. These oscillations result from an interplay between activation of alpha-1D calcium channels and BK calcium-dependent potassium channels. Variation in the kinetics of BK channels results from both alternative splicing and coassembly with beta subunits and gives rise to different frequencies of membrane potential oscillations, which vary systematically among hair cells of the same organ.
The ability of hair cells to signal stimuli of either polarity is preserved at the afferent synapse. This results in a steady release of neurotransmitters, which in turn results in a steady background firing in the fibers of the eighth nerve. Thus, receptor potentials of either polarity modulate calcium channel activity, and hence transmitter release.
A presynaptic electron-dense body, about 0. Neurotransmitter release is modulated with submillisecond precision to encode the frequency and intensity of sound and head movements. The excitatory amino acid glutamate has been shown to be released by hair cells, but it is not clear whether it is the primary transmitter or whether other transmitters are coreleased. The efferent synapse, carrying feedback control from the CNS via the olivocochlear fibers, uses acetylcholine as the transmitter.
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The synapse may be excitatory in some hair cells, but in most organs, efferent stimulation causes a slow, inhibitory hyperpolarization. The inhibition is caused by slow activation of calcium-dependent potassium channels SK. SK channels are voltage insensitive and can be activated by micromolar concentrations of calcium. The high calcium permeability of this receptor may permit sufficient calcium entry to activate SK calcium-dependent potassium channels, which in turn inhibits the cell.
Eatock, R. Springer handbook of auditory research. New York: Springer. Find this resource:. Effertz T. The how and why of identifying the hair cell mechano-electrical transduction channel. Pflugers Archive , , 73— Fekete, D. Development of the vertebrate ear: Insights from knockouts and mutants.
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Pflugers Archive Review , , 85— LeMasurier, M. Hair-cell mechanotransduction and cochlear amplification. Neuron , 48 , — Nayak, G. D, Ratnayaka, H. Development of the hair bundle and mechanotransduction. International Journal of Developmental Biology , 51 , — Pan B. The molecules that mediate sensory transduction in the mammalian inner ear. Current Opinion in Neurobiology , 34 , — Parsons, T. Synaptic ribbon. Conveyor belt or safety belt? Neuron , 37 , — Pepermans, E.
Oxford Research Encyclopedia of Neuroscience. Publications Pages Publications Pages. Oxford Research Encyclopedias Neuroscience. Search within subject: Select Cognitive Neuroscience Computational Neuroscience Development. Disorders of the Nervous System Invertebrate Neuroscience. Molecular and Cellular Systems Motor Systems. Auditory Hair Cells and Sensory Transduction.
Read More. Search within Show Summary Details View PDF Auditory Hair Cells and Sensory Transduction Summary and Keywords The organs of the vertebrate inner ear respond to a variety of mechanical stimuli: semicircular canals are sensitive to angular velocity, the saccule and utricle respond to linear acceleration including gravity , and the cochlea is sensitive to airborne vibration, or sound. The Mammalian Inner Ear The auditory and vestibular organs are formed during development by the unfolding of the otocyst, a spherical vesicle that gives rise to the inner ear.
Structure of the Hair Bundle Click to view larger Figure 1. Axis of Polarity The staircase-like variation in the heights of stereocilia Figures 1A, B confers a morphological axis of polarity to the bundle. The Mechanism of Transduction The last quarter-century has provided a good understanding of the mechanoelectrical transduction process, whereby deflections of the stereocilia cause the opening of transduction channels.
The Mechanotransduction Complex Mechanosensitive channels represent a third class of ion channel in addition to those gated by voltage and ligand binding. Molecular Basis of Hair Bundle Development Formation of the hair bundle during development is carefully orchestrated and presumably requires precisely timed expression of a large number of genes.
Cochlear Amplification Mechanical amplification of sound stimuli in mammals requires the activity of OHCs that reside in three rows along the entire length of the mammalian cochlea. Click to view larger Figure 2. The Receptor Potential Because mature hair cells lack voltage-gated sodium channels, they do not generate action potentials. Find this resource: Google Preview WorldCat. Jeffrey R. All rights reserved. Sign in to annotate.