Low‐frequency characteristics of intracellularly recorded receptor potentials in guinea‐pig cochlear hair cells.

Russell, Ian J.; Sellick, P.M.

doi:10.1113/jphysiol.1983.sp014668

Cited by 279 publications

(181 citation statements)

References 35 publications

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“…Open and filled symbols represent the apical-and basal-turn IHCs, respectively. tials recorded in vivo using sharp electrodes also show a phase lead approaching 0.25 cycle (90°) relative to BM displacement (Nuttall et al, 1981;Russell and Sellick, 1983;Dallos, 1985). These results are consistent with the notion that the IHC hairbundle displacement is related to BM velocity at low frequencies (Dallos et al, 1972).…”

Section: Input-output Functions Of Ihc Transducer Currentssupporting

confidence: 78%

“…As we show above (Crawford et al, 1991;Ricci et al, 2005), resting open probability of the MET channels is greater in low external Ca 2ϩ (Ricci et al, 1998). IHC receptor potentials recorded in vivo using sharp electrodes show a phase lead relative to BM displacement (Nuttall et al, 1981;Russell and Sellick, 1983;Dallos, 1985). We examined the phase relationship between the transducer current and BM displacement.…”

Section: Input-output Functions Of Ihc Transducer Currentsmentioning

confidence: 99%

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Mechanoelectric Transduction of Adult Inner Hair Cells

Song¹,

Dallos

He³

2007

J. Neurosci.

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Inner hair cells (IHCs) are the true sensory receptors in the cochlea; they transmit auditory information to the brain. IHCs respond to basilar membrane (BM) vibration by producing a transducer current through mechanotransducer (MET) channels located at the tip of their stereocilia when these are deflected. The IHC MET current has not been measured from adult animals. We simultaneously recorded IHC transducer currents and BM motion in a gerbil hemicochlea to examine relationships between these two variables and their variation along the cochlear length. Results show that although maximum transducer currents of IHCs are uniform along the cochlea, their operating range is graded and is narrower in the base. The MET current displays adaptation, which along with response magnitude depends on extracellular calcium concentration. The rate of adaptation is invariant along the cochlear length. We introduce a new method of measuring adaptation using sinusoidal stimuli. There is a phase lead of IHC transducer currents relative to sinusoidal BM displacement, reflecting viscoelastic coupling of their cilia and their adaptation process.

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Section: Input-output Functions Of Ihc Transducer Currentssupporting

confidence: 78%

Section: Input-output Functions Of Ihc Transducer Currentsmentioning

confidence: 99%

Mechanoelectric Transduction of Adult Inner Hair Cells

Song¹,

Dallos

He³

2007

J. Neurosci.

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“…We postulate that inactivation within the relatively depolarized operating range of IHCs (11,12) reduces the number of synaptic Ca V 1.3 channels available for stimulus-secretion coupling in the absence of CaBP2. Membrane capacitance (C m ) measurements turned out to be of limited help for understanding the effect of CaBP2 disruption on synaptic exocytosis.…”

Section: Discussionmentioning

confidence: 99%

Ca ²⁺ -binding protein 2 inhibits Ca ²⁺ -channel inactivation in mouse inner hair cells

Picher

Gehrt

Meese

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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Ca 2+ -binding protein 2 (CaBP2) inhibits the inactivation of heterologously expressed voltage-gated Ca 2+ channels of type 1.3 (Ca V 1.3) and is defective in human autosomal-recessive deafness 93 (DFNB93). Here, we report a newly identified mutation in CABP2 that causes a moderate hearing impairment likely via nonsense-mediated decay of CABP2-mRNA. To study the mechanism of hearing impairment resulting from CABP2 loss of function, we disrupted Cabp2 in mice (Cabp2 LacZ/LacZ ). CaBP2 was expressed by cochlear hair cells, preferentially in inner hair cells (IHCs), and was lacking from the postsynaptic spiral ganglion neurons (SGNs). Cabp2 LacZ/LacZ mice displayed intact cochlear amplification but impaired auditory brainstem responses. Patch-clamp recordings from Cabp2 LacZ/LacZ IHCs revealed enhanced Ca 2+ -channel inactivation. The voltage dependence of activation and the number of Ca 2+ channels appeared normal in Cabp2 LacZ/LacZ mice, as were ribbon synapse counts. Recordings from single SGNs showed reduced spontaneous and sound-evoked firing rates. We propose that CaBP2 inhibits Ca V 1.3 Ca 2+ -channel inactivation, and thus sustains the availability of Ca V 1.3 Ca 2+ channels for synaptic sound encoding. Therefore, we conclude that human deafness DFNB93 is an auditory synaptopathy.H earing relies on faithful transmission of information at ribbon synapses between inner hair cells (IHCs) and spiral ganglion neurons (SGNs; recently reviewed in refs. 1, 2). Ca 2+ channels at the IHC presynaptic active zone are key signaling elements because they couple the sound-evoked IHC receptor potential to the release of glutamate. IHC Ca 2+ -channel complexes are known to contain Ca V 1.3 α1 subunit (Cav1.3α1) (3-5), betasubunit 2 (Ca V β2) (6), and alpha2-delta subunit 2 (α2δ2) (7) to activate at around −60 mV (8-10), and are partially activated already at the IHC resting potential in vivo [thought to be between −55 and −45 mV (11, 12)], thereby mediating "spontaneous" glutamate release during silence (13).Compared with Ca V 1.3 channels studied in heterologous expression systems, Ca V 1.3 channels in IHCs show little inactivation, which has been attributed to inhibition of calmodulin-mediated Ca 2+ -dependent inactivation (CDI) (14-17) by Ca 2+ -binding proteins (CaBPs) (18,19) and/or the interaction of the distal and proximal regulatory domains of the Ca V 1.3α1 C terminus (20)(21)(22). This "noninactivating" phenotype of IHC Ca V 1.3 enables reliable excitation-secretion coupling during ongoing stimulation (23-25). In fact, postsynaptic spike rate adaptation during ongoing sound stimulation is thought to reflect primarily presynaptic vesicle pool depletion, with minor contributions of Ca V 1.3 inactivation or AMPA-receptor desensitization (23-26). CaBPs are calmodulin-like proteins that use three functional out of four helix-loop-helix domains (EF-hand) for Ca 2+ binding (27). They are thought to function primarily as signaling proteins (28) and differentially modulate calmodulin effectors (29,30). In addition, CaBPs m...

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“…CAP, an enhancement of the cochlear microphonic (CM) (Fex, 1959;Wiederhold and Peake, 1966), which reflects the summed receptor potentials of outer hair cells (Dallos, 1973;Russell and Sellick, 1983). To look for slow effects of OCB stimulation on the CM, we used moderate-level, 100 psec clicks, which allowed CM and CAP to be distinguished based on response latency (Fig.…”

Section: Similarities and Differences Between Fast And Slow Effectsmentioning

confidence: 99%

A novel cholinergic "slow effect" of efferent stimulation on cochlear potentials in the guinea pig

et al. 1995

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This report documents slow changes in cochlear responses produced by electrical stimulation of the olivocochlear bundle (OCB), which provides efferent innervation to the hair cells of the cochlea. These slow changes have time constants of 25–50 sec, three orders of magnitude slower than those reported previously. Such “slow effects” are similar to classically described “fast effects” in that (1) they comprise a suppression of the compound action potential (CAP) of the auditory nerve mirrored by an enhancement of the cochlear microphonic potential (CM) generated largely by the outer hair cells; (2) the magnitude of suppression decreases as the intensity of the acoustic stimulus increases; (3) they share the same dependence on OCB stimulation rate; (4) both are extinguished upon cutting the OCB; and (5) both are blocked with similar concentrations of a variety of cholinergic antagonists as well as with strychnine and bicuculline. These observations suggest that both fast and slow effects are mediated by the same receptor and are produced by conductance changes in outer hair cells. Slow effects differ from fast effects in that (1) fast effects are greatest for acoustic stimulus frequencies between 6 and 10 kHz, whereas slow effects peak for frequencies from 12 to 16 kHz, and (2) fast effects persist over long periods of OCB stimulation, whereas slow effects diminish after 60 sec of stimulation. The time course of the slow effects can be described mathematically by assuming that each shock-burst produces, in addition to a fast effect, a small decrease in CAP amplitude that decays exponentially with a time constant that is long relative to the intershock interval. The long time constant of the slow effect compared to the fast effect suggests that it may arise from a distinct intracellular mechanism, possibly mediated by second- messenger systems.

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Low‐frequency characteristics of intracellularly recorded receptor potentials in guinea‐pig cochlear hair cells.

Cited by 279 publications

References 35 publications

Mechanoelectric Transduction of Adult Inner Hair Cells

Mechanoelectric Transduction of Adult Inner Hair Cells

Ca ²⁺ -binding protein 2 inhibits Ca ²⁺ -channel inactivation in mouse inner hair cells

A novel cholinergic "slow effect" of efferent stimulation on cochlear potentials in the guinea pig

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Low‐frequency characteristics of intracellularly recorded receptor potentials in guinea‐pig cochlear hair cells.

Cited by 279 publications

References 35 publications

Mechanoelectric Transduction of Adult Inner Hair Cells

Mechanoelectric Transduction of Adult Inner Hair Cells

Ca 2+ -binding protein 2 inhibits Ca 2+ -channel inactivation in mouse inner hair cells

A novel cholinergic "slow effect" of efferent stimulation on cochlear potentials in the guinea pig

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Ca ²⁺ -binding protein 2 inhibits Ca ²⁺ -channel inactivation in mouse inner hair cells