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Full simulation on the dynamics of auditory synaptic fusion: Strong clustering of calcium channel might be the origin of the coherent release in the auditory hair cells

T0 review · 3 major / 5 minor · reviewed 2026-08-15 · deepseek-v4-flash

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Pith's one-line read The paper argues that strong clustering of CaV1.3 calcium channels synchronizes multivesicular release, producing the large monophasic EPSCs observed in auditory hair cells.

desk verdict The integrated simulation is a real piece of work, but the paper's central claim about channel clustering relies on simulations that do not yet reproduce the amplitude ordering it sets out to explain. read the letter →

arxiv 2505.07273 v1 pith:3DB4CCHQ submitted 2025-05-12 q-bio.NC physics.bio-ph

Jaeyun Yoo , Kang-Hun Ahn This is my paper · ORCID
classification q-bio.NCphysics.bio-ph
keywords haircellribbonsynapsemultivesicularreleasecalciumchannelclusteringCaV1.3EPSCwaveformssynapticvesiclefusionsimulationcochlearhearing
verification ladder T0 review T1 audit T2 compute T3 formal

The pith

A machine-rendered reading of the paper's core claim, the machinery that carries it, and where it could break.

The reading

This paper argues that the large, single-peaked electrical signals recorded at inner hair cell synapses come from several vesicles fusing at nearly the same time, not from one giant vesicle. The synchronizing agent, the authors propose, is strong local clustering of CaV1.3 calcium channels: a tight cluster admits a concentrated calcium cloud that binds the vesicle sensor and triggers coherent multivesicular release. The claim matters because it would settle a long-standing debate about the origin and shape of large EPSCs, and it would connect the physics of channel-channel interactions to hearing. The full simulation chain, from channel gating to AMPA receptor kinetics, reproduces the observed amplitude-over-charge pattern and shows that stronger clustering raises the amplitude of monophasic EPSCs.

What carries the argument

The load-bearing element is the spatial arrangement of CaV1.3 calcium channels, specifically tight sub-clusters within the active zone. The model couples a three-state Markov gating model of the channels, an analytic linearized-buffer solution for calcium diffusion from point sources, a five-calcium-ion sensor that triggers vesicle fusion, a fusion-pore expansion equation, and a 16-state AMPA receptor kinetic scheme. Strong clustering concentrates the calcium nanodomain so that several nearby vesicles reach the five-$\mathrm{Ca}^{2+}$ threshold within a narrow time window, generating a large, monophasic postsynaptic current.

What would settle it

Super-resolution or electron microscopy of inner hair cell active zones showing that CaV1.3 channels are not packed into sub-diffraction clusters would falsify the proposed mechanism; alternatively, an experiment that disrupts the presumed clustering forces without changing the large monophasic EPSC amplitude distribution would contradict the claim.

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Extended reading notes

Core claim

The paper's central discovery claim is that multivesicular release, driven by clustered CaV1.3 channels, can account for the large-amplitude monophasic EPSCs observed in inner hair cells, whereas univesicular release cannot plausibly explain the multiphasic EPSC shapes. In the simulations, weak clustering reproduces the experimentally known distributions of EPSC amplitude and charge, while strong clustering, modeled as tightly packed channels, produces higher local calcium concentrations and enhances monophasic EPSC amplitude. The authors conclude that a large EPSC is the summed postsynaptic response of several vesicles released nearly simultaneously, and that strong channel clustering is the mechanism that makes the release coherent. They report one residual discrepancy: in the current simulations multiphasic EPSC amplitudes still exceed monophasic ones, opposite to the experimental ordering, and they frame the result as a trend that stronger clustering would complete.

Load-bearing premise

The entire mechanism depends on CaV1.3 channels actually forming tight local clusters at inner hair cell active zones, which the paper assumes from depletion-interaction theory rather than demonstrates experimentally; if the channels are spread uniformly, the proposed synchronization does not occur.

Editorial extensions

If this is right

  • If the claim holds, large EPSCs in inner hair cells should be counted as compound events, so quantal analysis of these synapses would need to treat multivesicular sums as the elementary signal.
  • Monophasic and multiphasic EPSCs become two ends of a synchronization continuum, with the degree of calcium-channel clustering controlling the degree of vesicle synchrony.
  • The model's parameter sweep shows that fusion of three vesicles yields about 250 pA, matching the experimentally observed average EPSC amplitude and making multivesicular sums quantitatively consistent with measured amplitudes.
  • Univesicular release would require vesicles larger than those observed and cannot naturally generate multiphasic waveforms, so the simulation shifts the burden of explanation onto multivesicular release.
  • The apparent contradiction between the roughly 700 vesicles/s sustained release rate and the 200-400 spikes/s afferent firing rates becomes a well-posed question about how few vesicles need to fuse coherently to produce a large EPSC.

Reading between the lines

Editorial extensions of the paper, not claims the author makes directly.

  • If CaV1.3 clustering is a tunable property, interventions that alter channel mobility or the membrane environment could shift the balance between monophasic and multiphasic EPSCs, effectively changing temporal coding in the auditory nerve.
  • The same clustering-synchronization logic might apply to other ribbon synapses, such as retinal bipolar cells or vestibular hair cells, where large EPSCs have been reported; a simulation using their channel densities would be a direct test.
  • A specific prediction is that the amplitude distribution of monophasic EPSCs should correlate with the measured degree of CaV1.3 sub-clustering across developmental stages or experimental manipulations.
  • The residual sign discrepancy between simulated and experimental amplitude ordering suggests that, in addition to presynaptic clustering, a postsynaptic ingredient such as receptor saturation or desensitization shaped by the glutamate transient may be needed to complete the explanation.
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Editorial analysis

A structured set of objections, weighed in public.

Desk editor's note, referee report, and a circularity audit.

Referee Report

3 major / 5 minor

Summary. The manuscript presents a multiscale computational model of synaptic vesicle fusion at inner hair cell ribbon synapses, coupling CaV1.3 channel gating, buffered Ca2+ diffusion, a five-Ca2+-binding synaptotagmin-like sensor, vesicle fusion pore expansion, glutamate release, and a 16-state AMPA receptor model. The authors compare simulated EPSC amplitude versus charge distributions against experimental data from Chapochnikov et al. (Ref. 11) under two hypothesized spatial organizations of calcium channels: weak and strong clustering. They argue that strong clustering synchronizes multivesicular release and thereby explains large monophasic EPSCs, favoring multivesicular release over univesicular release as the origin of large EPSCs.

Significance. If the central claim could be established, the paper would offer a unified mechanistic account of two puzzling features of inner hair cell EPSCs—the coexistence of monophasic and multiphasic waveforms and the unusually large amplitudes of monophasic events—without invoking oversized vesicles. The authors are to be credited for building an unusually complete forward simulation chain from Ca2+ microdomains to postsynaptic currents and for comparing against quantitative experimental distributions (Fig. 2c). However, the key mechanistic prediction is not actually exhibited by the simulations as run: the strong-clustering results still show monophasic amplitudes below multiphasic ones. The claim therefore currently rests on an extrapolation beyond the parameter range that the authors simulated, which is a load-bearing gap.

major comments (3)
  1. [Section II, Figs. 2c and 3d] The experimental target, as stated in the text, is that multiphasic EPSC amplitudes are lower than monophasic amplitudes. The weak-clustering simulation (Fig. 2, right) shows the opposite ordering, and the strong-clustering run (Fig. 3d) does not reverse it; the authors concede that "the amplitude of monophasic EPSCs does not yet exceed that of multiphasic EPSCs in the current simulation results." The concluding claim that strong clustering can produce large-amplitude monophasic EPSCs is therefore an extrapolation rather than a demonstrated result. Please run simulations in a stronger clustering regime and show that the ordering flips, or soften the conclusion to match the data.
  2. [Section III.2 and Fig. 3a] The "strong clustering" condition is not parameterized. The text states only that weak clustering corresponds to a 25 nm inter-channel distance, but no inter-channel spacing, number of channels per cluster, or cluster geometry is given for the strong-clustering case. Without these values, the reader cannot assess how extreme the hypothesized clustering is, nor reproduce the simulations. Please state the geometric parameters for both conditions.
  3. [Section III.2, Eqs. (10)-(11)] The analytic Ca2+ solution introduces an ad hoc correction factor eta = 0.19 sqrt(r/r0 - 1) + 1, inserted to account for the ribbon ceiling. The manuscript says this reduces the difference between analytic and numerical solutions, but no derivation or sensitivity analysis is provided. Because this factor scales the entire Ca2+ transient, it can affect vesicle fusion timing and hence EPSC shape and amplitude. Please either derive eta from the boundary conditions or evaluate the sensitivity of the main results to its functional form.
minor comments (5)
  1. [Section III, first paragraph] There are several typos: "potasium" and "pottasium" should be "potassium," and "subsequant" should be "subsequent."
  2. [Table 2] The resting calcium concentration is listed as 5 x 10^5 mM, which is physically impossible; it should presumably be 5 x 10^-5 mM (50 nM). Also, the units for dCa2+ are written as s/m^2 but should be m^2/s.
  3. [Abstract] The phrase "strong calcium channeling of the calcium channel clusters" is awkward and presumably should be "strong clustering of calcium channels."
  4. [Section II and Fig. 2] The caption for Fig. 2c does not clearly identify which panel is experimental and which is simulated; please label the panels explicitly in the figure or caption.
  5. [General] No code or data availability statement is provided. For a simulation paper with many parameters, making the code available would substantially aid reproducibility and trust in the results.

Circularity Check

0 steps flagged · score 0.0 of 10

No circularity: EPSC predictions are forward-simulated from experimentally measured parameters and are not fitted to the target EPSC data.

full rationale

The paper's claimed output is the amplitude, charge, and monophasic/multiphasic shape of EPSCs. These are produced by a forward simulation chain: calcium-channel gating (Eqs. 1-7), buffered calcium diffusion (Eqs. 9-11), the five-calcium-ion sensor model taken from Beutner et al. (Ref. 31), fusion-pore expansion (Eq. 12), vesicular ion discharge (Eqs. 13-17), and a 16-state AMPA-receptor model. No component is fitted to the experimental EPSC amplitudes or to the monophasic/multiphasic ordering that the paper aims to explain. The authors explicitly report that the weak-clustering simulation gives the opposite ordering from experiments, and that even the strong-clustering run does not yet make monophasic EPSCs exceed multiphasic ones: 'Although the amplitude of monophasic EPSCs does not yet exceed that of multiphasic EPSCs in the current simulation results, it is evident that increased clustering of calcium channels leads to a clear enhancement in the amplitude of monophasic EPSCs.' A simulation that fails to match the target pattern cannot be a fitted-input prediction, because fitting would have forced agreement. The sensor model inherited from Ref. 31 was fitted to calcium-dependent exocytosis, not to EPSC shape, and the EPSC amplitude prediction additionally depends on independent submodels for pore opening, vesicle size, glutamate transport, and AMPA desensitization, so the output is not statistically forced by that upstream fit. The clustering assumption is explicitly introduced as a hypothesis ('we conduct simulations under the hypothesis that attractive interactions among calcium channels could give rise to strong clustering'), not derived from EPSC data. There are no load-bearing self-citations and no imported uniqueness theorems. The paper's main weakness is that the 'strong' clustering geometry is not quantitatively parameterized and the conclusion extrapolates beyond the computed parameter range; that is a correctness or completeness gap, not circularity. Therefore no circular step meets the evidentiary standard required by the review instructions.

Assumptions & free parameters 2 free parameters · 5 assumptions · 0 invented entities

The model rests on multiple experimentally derived parameters and modeling assumptions; the key ad hoc elements are the clustering geometry and the correction term η, plus the immediate-fusion simplification. No new physical entities are introduced.

free parameters (2)
  • calcium channel clustering strength = not quantified; qualitative comparison between weak (25 nm spacing) and strong
    The paper varies the spatial distribution of channels between 'weak' and 'strong' clustering without a precise calibrated value for the strong case. The central result depends on this choice, but it is not fitted to experimental EPSC data; it is a hypothesis-driven variable.
  • η ceiling correction factor = η = 0.19*sqrt(r/r0 - 1) + 1 (approximate, from Eq. 10)
    Inserted into the analytic calcium diffusion solution 'to reduce the difference in Fig.3' (matching analytic to numerical solutions). This is an ad hoc tuning parameter that affects the calcium concentration profile near the ceiling and hence fusion timing.
assumptions (5)
  • domain assumption Linearized buffer approximation for calcium diffusion (Eq. 9, from Ref. 29) is valid in the presynaptic microdomain.
    The model treats buffers with linearized reaction terms and replaces the diffusion matrix by a scalar dCa2+. This approximation is inherited from the literature but is load-bearing for the spatial spread of calcium and thus fusion timing.
  • ad hoc to paper Vesicle fusion occurs instantly when the calcium sensor binds its fifth calcium ion (Section III.3).
    The authors explicitly assume immediate fusion at the 5th Ca2+ binding, acknowledging that earlier models used a probabilistic fusion step and that this simplification 'causes problems in this part'. This directly shapes EPSC rise time and multiphasic structure.
  • domain assumption CaV1.3 channel gating follows the three-state Markov chain in Eq. (1) with rate constants tied to τact and open probability.
    This is a standard biophysical model, but its parameters come from whole-cell recordings in gerbil inner hair cells and are applied to rat spontaneous conditions; any mismatch in kinetics affects the timing of channel opening and thus the EPSC.
  • domain assumption Strong clustering of calcium channels can arise from depletion interactions between membrane proteins (Refs. 14-16).
    The entire strong-clustering scenario is motivated by polymer brush-induced depletion forces, not by direct evidence that CaV1.3 channels form tight clusters in vivo. If these interactions do not produce the assumed geometry, the central conclusion is moot.
  • domain assumption Glutamate transporters in the synaptic cleft are negligible for shaping the simulated EPSC (Section III.4).
    The authors justify this by distance arguments, but transporter activity could alter glutamate concentration profiles and hence receptor activation, affecting the amplitude and time course of EPSCs.

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Pith. "Pith review of Full simulation on the dynamics of auditory synaptic fusion: Strong clustering of calcium channel might be the origin of the coherent release in the auditory hair cells." pith.science (2026). https://pith.science/paper/3DB4CCHQ

@misc{pith2026250507273,
  author       = {Pith},
  title        = {Pith review of: Full simulation on the dynamics of auditory synaptic fusion: Strong clustering of calcium channel might be the origin of the coherent release in the auditory hair cells},
  year         = {2026},
  howpublished = {\url{https://pith.science/paper/3DB4CCHQ}},
  note         = {Machine review of arXiv:2505.07273}
}
read the original abstract

The precise timing of synaptic transmission in auditory hair cells is important to hearing and speech recognition. Neurotransmitter release is an underlying step in translating sound. Thus, understanding nature of the synaptic fusion is key to understand the hearing mechanism. Extraordinary large excitatory postsynaptic currents (EPSCs) have been observed in the auditory hair cell synapse, and its origin has been controversial. It is not known yet whether the size and shape of the EPSCs are results of a big vesicle or many small vesicles. We report our numerical simulation of the vesicular fusion process from calcium channel process to the generation of EPSC currents. Our numerical experiments indicate that the origin of the large EPSC with its mysterious form is close to the scenario of the multivesicular release. The large EPSCs might be triggered by strong calcium channeling of the calcium channel clusters.

Figures

Figures reproduced from arXiv: 2505.07273 by the authors.

Figure 1
Figure 1. a) Schematic of the structure of auditory neurons and inner hair cells. b) Schematic of calcium channel clusters. [PITH_FULL_IMAGE:figures/full_fig_p002_1.png] view at source ↗
Figure 2
Figure 2. Feature comparison between experimental results and simulation. a) In experiments, the first peak is the largest [PITH_FULL_IMAGE:figures/full_fig_p003_2.png] view at source ↗
Figure 3
Figure 3. a) The structure of calcium channel clusters. Both conditions when calcium channels are sparse and dense are [PITH_FULL_IMAGE:figures/full_fig_p004_3.png] view at source ↗
Figures from the paper (2 more)
Figure 4
Figure 4. Figure 4: a) The plot of EPSC amplitude when the pore opening rate and vesicle radius change. Over [PITH_FULL_IMAGE:figures/full_fig_p006_4.png]
Figure 5
Figure 5. Figure 5: a) Schematic of vesicle fusion model. There are glutamate and potassium inside the vesicle, and sodium and chlorin in [PITH_FULL_IMAGE:figures/full_fig_p008_5.png]

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Reference graph

Works this paper leans on

44 extracted references · 43 canonical work pages

  1. [1]

    ”Quantal analysis of synaptic potentials in neurons of the central nervous system.” Physiological reviews 70.1 (1990): 165-198

    Redman, Stephen. ”Quantal analysis of synaptic potentials in neurons of the central nervous system.” Physiological reviews 70.1 (1990): 165-198

    work page 1990

  2. [2]

    I., et al

    Guly´ as, A. I., et al. ”Hippocampal pyramidal cells excite inhibitory neurons through a single release site.” Nature 366.6456 (1993): 683

    work page 1993

  3. [3]

    Josh, and Chris J

    Lawrence, J. Josh, and Chris J. McBain. ”Interneuron diversity series: containing the detonation–feedforward inhibition in the CA3 hippocampus.” Trends in neurosciences 26.11 (2003): 631-640

    work page 2003

  4. [4]

    Angus, et al

    Silver, R. Angus, et al. ”High-probability uniquantal transmission at excitatory synapses in barrel cortex.” Science 302.5652 (2003): 1981-1984

    work page 2003

  5. [5]

    ”Sensory neuron signaling to the brain: properties of transmitter release from olfactory nerve terminals.” Journal of Neuroscience 24.12 (2004): 3023-3030

    Murphy, Gabe J., et al. ”Sensory neuron signaling to the brain: properties of transmitter release from olfactory nerve terminals.” Journal of Neuroscience 24.12 (2004): 3023-3030

    work page 2004

  6. [6]

    Holderith, and Zoltan Nusser

    Bir´ o,´Agota A., No´ emi B. Holderith, and Zoltan Nusser. ”Quantal size is independent of the release probability at hip- pocampal excitatory synapses.” Journal of Neuroscience 25.1 (2005): 223-232

    work page 2005

  7. [7]

    Tong, Gang, and Craig E. Jahr. ”Multivesicular release from excitatory synapses of cultured hippocampal neurons.” Neuron 12.1 (1994): 51-59

    work page 1994

  8. [8]

    ”Structure and function of the hair cell ribbon synapse.” The Journal of membrane biology 209.2-3 (2006): 153-165

    Nouvian, R´ egis, et al. ”Structure and function of the hair cell ribbon synapse.” The Journal of membrane biology 209.2-3 (2006): 153-165

    work page 2006

Show all 44 references
  1. [9]

    Glowatzki, Elisabeth, and Paul A. Fuchs. ”Transmitter release at the hair cell ribbon synapse.” Nature neuroscience 5.2 (2002): 147

    2002

  2. [10]

    ”Two modes of release shape the postsynaptic response at the inner hair cell ribbon synapse.” Journal of Neuroscience 30.12 (2010): 4210-4220

    Grant, Lisa, Eunyoung Yi, and Elisabeth Glowatzki. ”Two modes of release shape the postsynaptic response at the inner hair cell ribbon synapse.” Journal of Neuroscience 30.12 (2010): 4210-4220

    2010

  3. [11]

    ”Uniquantal release through a dynamic fusion pore is a candidate mechanism of hair cell exocytosis.” Neuron 83.6 (2014): 1389-1403

    Chapochnikov, Nikolai M., et al. ”Uniquantal release through a dynamic fusion pore is a candidate mechanism of hair cell exocytosis.” Neuron 83.6 (2014): 1389-1403

    2014

  4. [12]

    ”Interaction of a calcium channel blocker with noise in cochlear function in guinea pig.” Acta oto- laryngologica 132.11 (2012): 1140-1144

    Liu, Jun, et al. ”Interaction of a calcium channel blocker with noise in cochlear function in guinea pig.” Acta oto- laryngologica 132.11 (2012): 1140-1144

    2012

  5. [13]

    ”Developmental refinement of hair cell synapses tightens the coupling of Ca2+ influx to exocytosis.” The EMBO journal 33.3 (2014): 247-264

    Wong, Aaron B., et al. ”Developmental refinement of hair cell synapses tightens the coupling of Ca2+ influx to exocytosis.” The EMBO journal 33.3 (2014): 247-264

    2014

  6. [14]

    Asakura and F

    S. Asakura and F. Oosawa, J. Chem. Phys. 22, 1255 (1954)

    1954

  7. [15]

    Asakura and F

    S. Asakura and F. Oosawa, J. Polym. Sci. 33, 183 (1958)

    1958

  8. [16]

    ”Polymer brush-induced depletion interactions and clustering of membrane proteins.” The Journal of Chemical Physics 154.21 (2021): 214901

    Tom, Anvy Moly, Won Kyu Kim, and Changbong Hyeon. ”Polymer brush-induced depletion interactions and clustering of membrane proteins.” The Journal of Chemical Physics 154.21 (2021): 214901

    2021

  9. [17]

    ”The Ca2+ channel subunit β2 regulates Ca2+ channel abundance and function in inner hair cells and is required for hearing.” Journal of Neuroscience 29.34 (2009): 10730-10740

    Neef, Jakob, et al. ”The Ca2+ channel subunit β2 regulates Ca2+ channel abundance and function in inner hair cells and is required for hearing.” Journal of Neuroscience 29.34 (2009): 10730-10740

    2009

  10. [18]

    ”Individual synaptic vesicles mediate stimulated exocytosis from cochlear inner hair cells.” Proceedings of the National Academy of Sciences 115.50 (2018): 12811-12816

    Grabner, Chad Paul, and Tobias Moser. ”Individual synaptic vesicles mediate stimulated exocytosis from cochlear inner hair cells.” Proceedings of the National Academy of Sciences 115.50 (2018): 12811-12816

    2018

  11. [19]

    ”Probing the mechanism of exocytosis at the hair cell ribbon synapse.” Journal of Neuroscience 27.47 (2007): 12933-12944

    Neef, Andreas, et al. ”Probing the mechanism of exocytosis at the hair cell ribbon synapse.” Journal of Neuroscience 27.47 (2007): 12933-12944

    2007

  12. [20]

    ”Hearing requires otoferlin-dependent efficient replenishment of synaptic vesicles in hair cells.” Nature neuroscience 13.7 (2010): 869

    Pangrˇ siˇ c, Tina, et al. ”Hearing requires otoferlin-dependent efficient replenishment of synaptic vesicles in hair cells.” Nature neuroscience 13.7 (2010): 869

    2010

  13. [21]

    Charles Liberman

    Taberner, Annette M., and M. Charles Liberman. ”Response properties of single auditory nerve fibers in the mouse.” Journal of neurophysiology 93.1 (2005): 557-569

    2005

  14. [22]

    Magistretti, Jacopo, et al. ”Elementary properties of Ca2+ channels and their influence on multivesicular release and phase-locking at auditory hair cell ribbon synapses.” Frontiers in cellular neuroscience 9 (2015): 123

    2015

  15. [23]

    Moser, T., Brandt, A., and Lysakowski, A. (2006). Hair cell ribbon synapses. Cell and tissue research , 326(2), 347-359

    2006

  16. [24]

    ”Clustered Ca2+ channels are blocked by synaptic vesicle proton release at mammalian auditory ribbon synapses.” Cell reports 25.12 (2018): 3451-3464

    Vincent, Philippe FY, et al. ”Clustered Ca2+ channels are blocked by synaptic vesicle proton release at mammalian auditory ribbon synapses.” Cell reports 25.12 (2018): 3451-3464

    2018

  17. [25]

    ”Cell-type-specific tuning of Cav1

    Scharinger, Anja, et al. ”Cell-type-specific tuning of Cav1. 3 Ca2+-channels by a C-terminal automodulatory domain.” Frontiers in cellular neuroscience 9 (2015): 309

    2015

  18. [26]

    ”Subneuronal Processing of Information by Solitary Waves and Stochastic Processes.” Nano and Molecular Electronics Handbook

    Lyshevski, Sergey Edward. ”Subneuronal Processing of Information by Solitary Waves and Stochastic Processes.” Nano and Molecular Electronics Handbook. CRC Press, 2018. 582-623

    2018

  19. [27]

    ”Biophysical properties of CaV1

    Johnson, Stuart L., and Walter Marcotti. ”Biophysical properties of CaV1. 3 calcium channels in gerbil inner hair cells.” The Journal of physiology 586.4 (2008): 1029-1042

    2008

  20. [28]

    ”Burst activity and ultrafast activation kinetics of CaV1

    Zampini, Valeria, et al. ”Burst activity and ultrafast activation kinetics of CaV1. 3 Ca2+ channels support presynaptic activity in adult gerbil hair cell ribbon synapses.” The Journal of physiology 591.16 (2013): 3811-3820

    2013

  21. [29]

    Naraghi, Mohammad, and Erwin Neher. ”Linearized buffered Ca2+ diffusion in microdomains and its implications for calculation of [Ca2+] at the mouth of a calcium channel.” Journal of Neuroscience 17.18 (1997): 6961-6973

    1997

  22. [30]

    ”Nanodomain Ca2+ of Ca2+ channels detected by a tethered genetically encoded Ca2+ sensor.” Nature communications 3 (2012): 778

    Tay, Lai Hock, et al. ”Nanodomain Ca2+ of Ca2+ channels detected by a tethered genetically encoded Ca2+ sensor.” Nature communications 3 (2012): 778

    2012

  23. [31]

    ”Calcium dependence of exocytosis and endocytosis at the cochlear inner hair cell afferent synapse.” Neuron 29.3 (2001): 681-690

    Beutner, Dirk, et al. ”Calcium dependence of exocytosis and endocytosis at the cochlear inner hair cell afferent synapse.” Neuron 29.3 (2001): 681-690

    2001

  24. [32]

    ”A mechanism for discharge of charged excitatory neurotransmitter.” Bio- 11 physical journal 72.2 (1997): 507-521

    Khanin, Raya, Hanna Parnas, and Lee Segel. ”A mechanism for discharge of charged excitatory neurotransmitter.” Bio- 11 physical journal 72.2 (1997): 507-521

    1997

  25. [33]

    Bouteiller, Jean-Marie C., et al. ”Integrated multiscale modeling of the nervous system: predicting changes in hippocampal network activity by a positive AMPA receptor modulator.” IEEE transactions on biomedical engineering 58.10 (2011): 3008-3011

    2011

  26. [34]

    Robert, Antoine, and James R. Howe. ”How AMPA receptor desensitization depends on receptor occupancy.” Journal of Neuroscience 23.3 (2003): 847-858

    2003

  27. [35]

    ”Resolving the structure of inner ear ribbon synapses with STED microscopy.” Synapse 69.5 (2015): 242-255

    Rutherford, Mark A. ”Resolving the structure of inner ear ribbon synapses with STED microscopy.” Synapse 69.5 (2015): 242-255

    2015

  28. [36]

    Bertil, Hille, and H. Bertil. ”Ion channels of excitable membranes.” Sunderland, Mass.: Sinauer Associates. 3rd Edi- tion.–2007 (2001)

    2001

  29. [37]

    ”Otoferlin, defective in a human deafness form, is essential for exocytosis at the auditory ribbon synapse.” Cell 127.2 (2006): 277-289

    Roux, Isabelle, et al. ”Otoferlin, defective in a human deafness form, is essential for exocytosis at the auditory ribbon synapse.” Cell 127.2 (2006): 277-289

    2006

  30. [38]

    Basic neurochemistry: principles of molecular, cellular, and medical neurobiology

    Brady, Scott, et al., eds. Basic neurochemistry: principles of molecular, cellular, and medical neurobiology. Academic press, 2011

    2011

  31. [39]

    ”Sodium and calcium currents shape action potentials in immature mouse inner hair cells.” The Journal of physiology 552.3 (2003): 743-761

    Marcotti, Walter, et al. ”Sodium and calcium currents shape action potentials in immature mouse inner hair cells.” The Journal of physiology 552.3 (2003): 743-761

    2003

  32. [40]

    ”Determining the neurotransmitter concentration profile at active synapses.” Molec- ular neurobiology 40.3 (2009): 289-306

    Scimemi, Annalisa, and Marco Beato. ”Determining the neurotransmitter concentration profile at active synapses.” Molec- ular neurobiology 40.3 (2009): 289-306

    2009

  33. [41]

    Zylbertal, Asaph, Yosef Yarom, and Shlomo Wagner. ”The Slow Dynamics of Intracellular Sodium Concentration Increase the Time Window of Neuronal Integration: A Simulation Study.” Frontiers in computational neuroscience 11 (2017): 85

    2017

  34. [42]

    Wierenga, and Hilgo Bruining

    Schulte, Joran T., Corette J. Wierenga, and Hilgo Bruining. ”Chloride transporters and GABA polarity in developmental, neurological and psychiatric conditions.” Neuroscience & Biobehavioral Reviews 90 (2018): 260-271

    2018

  35. [43]

    ”Hair cell synaptic ribbons are essential for synchronous auditory signalling.” Nature 434.7035 (2005): 889

    Khimich, Darina, et al. ”Hair cell synaptic ribbons are essential for synchronous auditory signalling.” Nature 434.7035 (2005): 889

    2005

  36. [44]

    ”The origin of quantal size variation: vesicular glutamate concentration plays a significant role.” Journal of Neuroscience 27.11 (2007): 3046-3056

    Wu, Xin-Sheng, et al. ”The origin of quantal size variation: vesicular glutamate concentration plays a significant role.” Journal of Neuroscience 27.11 (2007): 3046-3056. 12 Parameter Value Unit gmax 3.8 nS Vrev -23.4 mV V 1 2 38 mV S 8 mV Table 1. Parameters for calcium chann...

    2007

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