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In this article, we study the neural encoding of acoustic information for FM-bats (such as Eptesicus fuscus) in simulation. In echolocation research, the frequency–time sound representation as expressed by the spectrogram is often
considered as input. The rationale behind this is that a similar representation is present in the cochlea, i.e. the receptor
potential of the inner hair cells (IHC) along the length of the cochlea, and hence similar acoustic information is relayed
to the brain. In this article, we study to what extent the latter assumption is true. The receptor potential is converted
into neural activity of the synapting auditory nerve cells (ANC), and information might be lost in this conversion process.
Especially for FM-bats, this information transmission is not trivial: in contrast to other mammals, they detect short transient
signals, and consequently neural activity can only be integrated over very limited time intervals. To quantify the amount
of information transmitted we design a neural network-based algorithm to reconstruct the IHC receptor potentials from the
spiking activity of the synapting auditory neurons. Both the receptor potential and the resulting neural activity are simulated
using Meddis’ peripheral model. Comparing the reconstruction to the IHC receptor potential, we quantify the information transmission
of the bat hearing system and investigate how this depends on the intensity of the incoming signal, the distribution of auditory
neurons, and previous masking stimulation (adaptation). In addition, we show how this approach allows to inspect which spectral
features survive neural encoding and hence can be relevant for echolocation. 相似文献
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Joshua H. Goldwyn Eric Shea-Brown Jay T. Rubinstein 《Journal of computational neuroscience》2010,28(3):405-424
Cochlear implant speech processors stimulate the auditory nerve by delivering amplitude-modulated electrical pulse trains
to intracochlear electrodes. Studying how auditory nerve cells encode modulation information is of fundamental importance,
therefore, to understanding cochlear implant function and improving speech perception in cochlear implant users. In this paper,
we analyze simulated responses of the auditory nerve to amplitude-modulated cochlear implant stimuli using a point process
model. First, we quantify the information encoded in the spike trains by testing an ideal observer’s ability to detect amplitude
modulation in a two-alternative forced-choice task. We vary the amount of information available to the observer to probe how
spike timing and averaged firing rate encode modulation. Second, we construct a neural decoding method that predicts several
qualitative trends observed in psychophysical tests of amplitude modulation detection in cochlear implant listeners. We find
that modulation information is primarily available in the sequence of spike times. The performance of an ideal observer, however,
is inconsistent with observed trends in psychophysical data. Using a neural decoding method that jitters spike times to degrade
its temporal resolution and then computes a common measure of phase locking from spike trains of a heterogeneous population
of model nerve cells, we predict the correct qualitative dependence of modulation detection thresholds on modulation frequency
and stimulus level. The decoder does not predict the observed loss of modulation sensitivity at high carrier pulse rates,
but this framework can be applied to future models that better represent auditory nerve responses to high carrier pulse rate
stimuli. The supplemental material of this article contains the article’s data in an active, re-usable format. 相似文献
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Stimulus presentation is believed to quench neural response variability as measured by fano-factor (FF). However, the relative contributions of within-trial spike irregularity and trial-to-trial rate variability to FF fluctuations have remained elusive. Here, we introduce a principled approach for accurate estimation of spiking irregularity and rate variability in time for doubly stochastic point processes. Consistent with previous evidence, analysis showed stimulus-induced reduction in rate variability across multiple cortical and subcortical areas. However, unlike what was previously thought, spiking irregularity, was not constant in time but could be enhanced due to factors such as bursting abating the quench in the post-stimulus FF. Simulations confirmed plausibility of a time varying spiking irregularity arising from within and between pool correlations of excitatory and inhibitory neural inputs. By accurate parsing of neural variability, our approach reveals previously unnoticed changes in neural response variability and constrains candidate mechanisms that give rise to observed rate variability and spiking irregularity within brain regions. 相似文献
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Adult Bengalese finches generate a variable song that obeys a distinct and individual syntax. The syntax is gradually lost
over a period of days after deafening and is recovered when hearing is restored. We present a spiking neuronal network model
of the song syntax generation and its loss, based on the assumption that the syntax is stored in reafferent connections from
the auditory to the motor control area. Propagating synfire activity in the HVC codes for individual syllables of the song
and priming signals from the auditory network reduce the competition between syllables to allow only those transitions that
are permitted by the syntax. Both imprinting of song syntax within HVC and the interaction of the reafferent signal with an
efference copy of the motor command are sufficient to explain the gradual loss of syntax in the absence of auditory feedback.
The model also reproduces for the first time experimental findings on the influence of altered auditory feedback on the song
syntax generation, and predicts song- and species-specific low frequency components in the LFP. This study illustrates how
sequential compositionality following a defined syntax can be realized in networks of spiking neurons. 相似文献
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Visual cues often modulate auditory signal processing, leading to improved sound detection. However, the synaptic and circuit mechanism underlying this cross-modal modulation remains poorly understood. Using larval zebrafish, we first established a cross-modal behavioral paradigm in which a preceding flash enhances sound-evoked escape behavior, which is known to be executed through auditory afferents (VIII(th) nerves) and command-like neurons (Mauthner cells). In?vivo recording revealed that the visual enhancement of auditory escape is achieved by increasing sound-evoked Mauthner cell responses. This increase in Mauthner cell responses is accounted for by the increase in the signal-to-noise ratio of sound-evoked VIII(th) nerve spiking and efficacy of VIII(th) nerve-Mauthner cell synapses. Furthermore, the visual enhancement of Mauthner cell response and escape behavior requires light-responsive dopaminergic neurons in the caudal hypothalamus and D1 dopamine receptor activation. Our findings illustrate a cooperative neural mechanism for visual modulation of audiomotor processing that involves dopaminergic neuromodulation. 相似文献
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We present a rate model of the spontaneous activity in the auditory cortex, based on synaptic depression. A Stochastic integro-differential
system of equations is derived and the analysis reveals two main regimes. The first regime corresponds to a normal activity.
The second regime corresponds to epileptic spiking. A detailed analysis of each regime is presented and we prove in particular
that synaptic depression stabilizes the global cortical dynamics. The transition between the two regimes is induced by a change
in synaptic connectivity: when the overall connectivity is strong enough, an epileptic activity is spontaneously generated.
Numerical simulations confirm the predictions of the theoretical analysis. In particular, our results explain the transition
from normal to epileptic regime which can be induced in rats auditory cortex, following a specific pairing protocol. A change
in the cortical maps reorganizes the synaptic connectivity and this transition between regimes is accounted for by our model.
We have used data from recording experiments to fit synaptic weight distributions. Simulations with the fitted distributions
are qualitatively similar to the real EEG recorded in vivo during the experiments.
We conclude that changes in the synaptic weight function in our model, which affects excitatory synapses organization and
reproduces the changes in cortical map connectivity can be understood as the main mechanism to explain the transitions of
the EEG from the normal to the epileptic regime in the auditory cortex.
D.H is incumbent to the Hass Russell Career Chair Development. 相似文献
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Frank Rattay Thomas Potrusil Cornelia Wenger Andrew K. Wise Rudolf Glueckert Anneliese Schrott-Fischer 《PloS one》2013,8(11)
Background
Our knowledge about the neural code in the auditory nerve is based to a large extent on experiments on cats. Several anatomical differences between auditory neurons in human and cat are expected to lead to functional differences in speed and safety of spike conduction.Methodology/Principal Findings
Confocal microscopy was used to systematically evaluate peripheral and central process diameters, commonness of myelination and morphology of spiral ganglion neurons (SGNs) along the cochlea of three human and three cats. Based on these morphometric data, model analysis reveales that spike conduction in SGNs is characterized by four phases: a postsynaptic delay, constant velocity in the peripheral process, a presomatic delay and constant velocity in the central process. The majority of SGNs are type I, connecting the inner hair cells with the brainstem. In contrast to those of humans, type I neurons of the cat are entirely myelinated. Biophysical model evaluation showed delayed and weak spikes in the human soma region as a consequence of a lack of myelin. The simulated spike conduction times are in accordance with normal interwave latencies from auditory brainstem response recordings from man and cat. Simulated 400 pA postsynaptic currents from inner hair cell ribbon synapses were 15 times above threshold. They enforced quick and synchronous spiking. Both of these properties were not present in type II cells as they receive fewer and much weaker (∼26 pA) synaptic stimuli.Conclusions/Significance
Wasting synaptic energy boosts spike initiation, which guarantees the rapid transmission of temporal fine structure of auditory signals. However, a lack of myelin in the soma regions of human type I neurons causes a large delay in spike conduction in comparison with cat neurons. The absent myelin, in combination with a longer peripheral process, causes quantitative differences of temporal parameters in the electrically stimulated human cochlea compared to the cat cochlea. 相似文献11.
Martinez D 《Biological cybernetics》2005,93(5):355-365
Across species, primary olfactory centers show similarities both in their cellular organization and their types of olfactory
information coding. In this article, we consider an excitatory-inhibitory spiking neural network as a model of early olfactory
systems (antennal lobe for insects, olfactory bulb for vertebrates). In line with experimental results, we show that, in our
network, odor-like stimuli evoke synchronization of excitatory cells, phase-locked to the oscillations of the local field
potential. As revealed by a mathematical analysis, the phase-locking probability of excitatory cells is given by an inverted-U
function and the firing probability of inhibitory cells is well described by a sigmoid function. These neural response functions
are used to reduce the spiking model to a more abstract model with discrete-time dynamics (oscillatory cycles) and binary-state
neurons (phase-locked or not). An iterative map, built for explaining the dynamics of the binary model, reveals that it converges
to fixed point attractors similar to those obtained with the spiking model. This result is consistent with odor-specific attractors
found in recent experimental studies. It also provides insights for designing bio-inspired olfactory associative memories
applicable for data analysis in electronic noses. 相似文献
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Christine Köppl Regina Nickel 《Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology》2007,193(6):613-624
Cochlear microphonics (CMs), which represent the electrical activity of hair cells, and compound action potentials (CAPs),
which represent the activity of the auditory nerve, were recorded from the round window of the inner ear, in owlets aged between
5 and 97 days posthatching, i.e., from soon after hatching to beyond fledgling. At the earliest ages examined, animals showed
very insensitive CM and virtually no CAP responses. Thus, hearing in barn owls develops entirely posthatching and the birds
appear to be profoundly deaf well into the second week. Thresholds improved gradually after that and CMs reached their adult
sensitivity at 5 weeks posthatching at all frequencies. Compound action potential responses appeared progressively later with
increasing frequency. Adult neural sensitivity was achieved about 1 week later than for the CM responses at most frequencies,
but took until 9–10 weeks posthatching at the highest frequencies (8–10 kHz). This indicates an apex-to-base maturation sequence
of neural sensitivity within the cochlea, with a disproportionately long period to maturity for the most basal regions. Compound
action potential amplitudes matured even later, at about 3 months posthatching, at all frequencies. This suggests a prolonged
immaturity in the temporal synchrony of spiking in the auditory nerve. 相似文献
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A model for firing of the auditory nerve fibres was carried out on a general purpose digital computer. In the model a noise with small correlation time and with assigned standard deviation (when modeling a spontaneous discharge) or a sum of a noise and a determinated signal (when modeling an elicited discharge) is compared with incremental threshold. When the threshold is exceeded a spike occurs and the threshold is increased. The threshold qualitative properties and quantitative values were chosen in a way to provide the most reliable patterns of spontaneous discharge, according to the literature data obtained from the cat's auditory nerve. When stimulated by tone-bursts the model reveals intrinsic ability of mimicking the phenomena of discharge rate short-term adaptation. Thus according to our model the short-term adaptation is entirely due to the properties of the incremental threshold. 相似文献
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Interaural time difference (ITD) is a major cue for sound azimuth localization at lower sound frequencies. We review two theories of how the sound localization neural circuit works. One of them proposes labeling of sound direction in the array of delay lines by maximal response of the tuning curve (Jeffress model). The other proposes detection of the direction by calculating the maximum slope of tuning curves. We formulate a simple hypothesis from this that stochastic neural response infers sound direction from this maximum slope, which supports the second theory. We calculate the output spike time density used in the readout of sound direction analytically. We show that the numerical implementation of the model yields results similar to those observed in experiments in mammals. We then go one step further and show that our model also gives similar results when a detailed implementation of the cochlear implant processor and simulation of implant to auditory nerve transduction are used, instead of the simplified model of auditory nerve input. Our results are useful in explaining some recent puzzling observations on the binaural cochlear implantees. 相似文献
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Maral Budak Karl Grosh Aritra Sasmal Gabriel Corfas Michal Zochowski Victoria Booth 《PLoS computational biology》2021,17(1)
Hidden hearing loss (HHL) is an auditory neuropathy characterized by normal hearing thresholds but reduced amplitudes of the sound-evoked auditory nerve compound action potential (CAP). In animal models, HHL can be caused by moderate noise exposure or aging, which induces loss of inner hair cell (IHC) synapses. In contrast, recent evidence has shown that transient loss of cochlear Schwann cells also causes permanent auditory deficits in mice with similarities to HHL. Histological analysis of the cochlea after auditory nerve remyelination showed a permanent disruption of the myelination patterns at the heminode of type I spiral ganglion neuron (SGN) peripheral terminals, suggesting that this defect could be contributing to HHL. To shed light on the mechanisms of different HHL scenarios observed in animals and to test their impact on type I SGN activity, we constructed a reduced biophysical model for a population of SGN peripheral axons whose activity is driven by a well-accepted model of cochlear sound processing. We found that the amplitudes of simulated sound-evoked SGN CAPs are lower and have greater latencies when heminodes are disorganized, i.e. they occur at different distances from the hair cell rather than at the same distance as in the normal cochlea. These results confirm that disruption of heminode positions causes desynchronization of SGN spikes leading to a loss of temporal resolution and reduction of the sound-evoked SGN CAP. Another mechanism resulting in HHL is loss of IHC synapses, i.e., synaptopathy. For comparison, we simulated synaptopathy by removing high threshold IHC-SGN synapses and found that the amplitude of simulated sound-evoked SGN CAPs decreases while latencies remain unchanged, as has been observed in noise exposed animals. Thus, model results illuminate diverse disruptions caused by synaptopathy and demyelination on neural activity in auditory processing that contribute to HHL as observed in animal models and that can contribute to perceptual deficits induced by nerve damage in humans. 相似文献
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Pain caused by nerve injury (i.e. neuropathic pain) is associated with development of neuronal hyperexcitability at several points along the pain pathway. Within primary afferents, numerous injury-induced changes have been identified but it remains unclear which molecular changes are necessary and sufficient to explain cellular hyperexcitability. To investigate this, we built computational models that reproduce the switch from a normal spiking pattern characterized by a single spike at the onset of depolarization to a neuropathic one characterized by repetitive spiking throughout depolarization. Parameter changes that were sufficient to switch the spiking pattern also enabled membrane potential oscillations and bursting, suggesting that all three pathological changes are mechanistically linked. Dynamical analysis confirmed this prediction by showing that excitability changes co-develop when the nonlinear mechanism responsible for spike initiation switches from a quasi-separatrix-crossing to a subcritical Hopf bifurcation. This switch stems from biophysical changes that bias competition between oppositely directed fast- and slow-activating conductances operating at subthreshold potentials. Competition between activation and inactivation of a single conductance can be similarly biased with equivalent consequences for excitability. "Bias" can arise from a multitude of molecular changes occurring alone or in combination; in the latter case, changes can add or offset one another. Thus, our results identify pathological change in the nonlinear interaction between processes affecting spike initiation as the critical determinant of how simple injury-induced changes at the molecular level manifest complex excitability changes at the cellular level. We demonstrate that multiple distinct molecular changes are sufficient to produce neuropathic changes in excitability; however, given that nerve injury elicits numerous molecular changes that may be individually sufficient to alter spike initiation, our results argue that no single molecular change is necessary to produce neuropathic excitability. This deeper understanding of degenerate causal relationships has important implications for how we understand and treat neuropathic pain. 相似文献
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Analysis of discharges recorded simultaneously from pairs of auditory nerve fibers. 总被引:2,自引:0,他引:2
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Spike trains were recorded simultaneously from pairs of auditory nerve fibres in anesthetized cats. Tests for correlation between spike trains were developed for spontaneous activity and for discharge patterns resulting from single-tone stimuli. The application of these tests to the recordings indicates that the responses of auditory nerve fibers to a tone and to silence can be described as statistically independent point processes. This result implies that the initiation of spikes in these fibers is governed by localized processes specific for each fiber. 相似文献
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A generalized linear model for estimating spectrotemporal receptive fields from responses to natural sounds 总被引:1,自引:0,他引:1
In the auditory system, the stimulus-response properties of single neurons are often described in terms of the spectrotemporal receptive field (STRF), a linear kernel relating the spectrogram of the sound stimulus to the instantaneous firing rate of the neuron. Several algorithms have been used to estimate STRFs from responses to natural stimuli; these algorithms differ in their functional models, cost functions, and regularization methods. Here, we characterize the stimulus-response function of auditory neurons using a generalized linear model (GLM). In this model, each cell's input is described by: 1) a stimulus filter (STRF); and 2) a post-spike filter, which captures dependencies on the neuron's spiking history. The output of the model is given by a series of spike trains rather than instantaneous firing rate, allowing the prediction of spike train responses to novel stimuli. We fit the model by maximum penalized likelihood to the spiking activity of zebra finch auditory midbrain neurons in response to conspecific vocalizations (songs) and modulation limited (ml) noise. We compare this model to normalized reverse correlation (NRC), the traditional method for STRF estimation, in terms of predictive power and the basic tuning properties of the estimated STRFs. We find that a GLM with a sparse prior predicts novel responses to both stimulus classes significantly better than NRC. Importantly, we find that STRFs from the two models derived from the same responses can differ substantially and that GLM STRFs are more consistent between stimulus classes than NRC STRFs. These results suggest that a GLM with a sparse prior provides a more accurate characterization of spectrotemporal tuning than does the NRC method when responses to complex sounds are studied in these neurons. 相似文献
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Identifying behaviorally relevant sounds in the presence of background noise is one of the most important and poorly understood challenges faced by the auditory system. An elegant solution to this problem would be for the auditory system to represent sounds in a noise-invariant fashion. Since a major effect of background noise is to alter the statistics of the sounds reaching the ear, noise-invariant representations could be promoted by neurons adapting to stimulus statistics. Here we investigated the extent of neuronal adaptation to the mean and contrast of auditory stimulation as one ascends the auditory pathway. We measured these forms of adaptation by presenting complex synthetic and natural sounds, recording neuronal responses in the inferior colliculus and primary fields of the auditory cortex of anaesthetized ferrets, and comparing these responses with a sophisticated model of the auditory nerve. We find that the strength of both forms of adaptation increases as one ascends the auditory pathway. To investigate whether this adaptation to stimulus statistics contributes to the construction of noise-invariant sound representations, we also presented complex, natural sounds embedded in stationary noise, and used a decoding approach to assess the noise tolerance of the neuronal population code. We find that the code for complex sounds in the periphery is affected more by the addition of noise than the cortical code. We also find that noise tolerance is correlated with adaptation to stimulus statistics, so that populations that show the strongest adaptation to stimulus statistics are also the most noise-tolerant. This suggests that the increase in adaptation to sound statistics from auditory nerve to midbrain to cortex is an important stage in the construction of noise-invariant sound representations in the higher auditory brain. 相似文献