Learning the Vector Coding of Egocentric Boundary Cells from Visual Data.

The use of spatial maps to navigate through the world requires a complex ongoing transformation of egocentric views of the environment into position within the allocentric map. Recent research has discovered neurons in retrosplenial cortex and other structures that could mediate the transformation from egocentric views to allocentric views. These egocentric boundary cells respond to the egocentric direction and distance of barriers relative to an animal's point of view. This egocentric coding based on the visual features of barriers would seem to require complex dynamics of cortical interactions. However, computational models presented here show that egocentric boundary cells can be generated with a remarkably simple synaptic learning rule that forms a sparse representation of visual input as an animal explores the environment. Simulation of this simple sparse synaptic modification generates a population of egocentric boundary cells with distributions of direction and distance coding that strikingly resemble those observed within the retrosplenial cortex. Furthermore, some egocentric boundary cells learnt by the model can still function in new environments without retraining. This provides a framework for understanding the properties of neuronal populations in the retrosplenial cortex that may be essential for interfacing egocentric sensory information with allocentric spatial maps of the world formed by neurons in downstream areas, including the grid cells in entorhinal cortex and place cells in the hippocampus.SIGNIFICANCE STATEMENT The computational model presented here demonstrates that the recently discovered egocentric boundary cells in retrosplenial cortex can be generated with a remarkably simple synaptic learning rule that forms a sparse representation of visual input as an animal explores the environment. Additionally, our model generates a population of egocentric boundary cells with distributions of direction and distance coding that strikingly resemble those observed within the retrosplenial cortex. This transformation between sensory input and egocentric representation in the navigational system could have implications for the way in which egocentric and allocentric representations interface in other brain areas.

Spike-timing dependent plasticity partially compensates for neural delays in a multi-layered network of motion-sensitive neurons.

The ability of the brain to represent the external world in real-time is impacted by the fact that neural processing takes time. Because neural delays accumulate as information progresses through the visual system, representations encoded at each hierarchical level are based upon input that is progressively outdated with respect to the external world. This 'representational lag' is particularly relevant to the task of localizing a moving object-because the object's location changes with time, neural representations of its location potentially lag behind its true location. Converging evidence suggests that the brain has evolved mechanisms that allow it to compensate for its inherent delays by extrapolating the position of moving objects along their trajectory. We have previously shown how spike-timing dependent plasticity (STDP) can achieve motion extrapolation in a two-layer, feedforward network of velocity-tuned neurons, by shifting the receptive fields of second layer neurons in the opposite direction to a moving stimulus. The current study extends this work by implementing two important changes to the network to bring it more into line with biology: we expanded the network to multiple layers to reflect the depth of the visual hierarchy, and we implemented more realistic synaptic time-courses. We investigate the accumulation of STDP-driven receptive field shifts across several layers, observing a velocity-dependent reduction in representational lag. These results highlight the role of STDP, operating purely along the feedforward pathway, as a developmental strategy for delay compensation.

Predictive Visual Motion Extrapolation Emerges Spontaneously and without Supervision at Each Layer of a Hierarchical Neural Network with Spike-Timing-Dependent Plasticity.

The fact that the transmission and processing of visual information in the brain takes time presents a problem for the accurate real-time localization of a moving object. One way this problem might be solved is extrapolation: using an object's past trajectory to predict its location in the present moment. Here, we investigate how a simulated in silico layered neural network might implement such extrapolation mechanisms, and how the necessary neural circuits might develop. We allowed an unsupervised hierarchical network of velocity-tuned neurons to learn its connectivity through spike-timing-dependent plasticity (STDP). We show that the temporal contingencies between the different neural populations that are activated by an object as it moves causes the receptive fields of higher-level neurons to shift in the direction opposite to their preferred direction of motion. The result is that neural populations spontaneously start to represent moving objects as being further along their trajectory than where they were physically detected. Because of the inherent delays of neural transmission, this effectively compensates for (part of) those delays by bringing the represented position of a moving object closer to its instantaneous position in the world. Finally, we show that this model accurately predicts the pattern of perceptual mislocalization that arises when human observers are required to localize a moving object relative to a flashed static object (the flash-lag effect; FLE).SIGNIFICANCE STATEMENT Our ability to track and respond to rapidly changing visual stimuli, such as a fast-moving tennis ball, indicates that the brain is capable of extrapolating the trajectory of a moving object to predict its current position, despite the delays that result from neural transmission. Here, we show how the neural circuits underlying this ability can be learned through spike-timing-dependent synaptic plasticity and that these circuits emerge spontaneously and without supervision. This demonstrates how the neural transmission delays can, in part, be compensated to implement the extrapolation mechanisms required to predict where a moving object is at the present moment.

Ambient air pollution and epileptic seizures: A panel study in Australia.

OBJECTIVE: Emerging evidence has shown that ambient air pollution affects brain health, but little is known about its effect on epileptic seizures. This work aimed to assess the association between daily exposure to ambient air pollution and the risk of epileptic seizures. METHODS: This study used epileptic seizure data from two independent data sources (NeuroVista and Seer App seizure diary). In the NeuroVista data set, 3273 seizures were recorded using intracranial electroencephalography (iEEG) from 15 participants with refractory focal epilepsy in Australia in 2010-2012. In the seizure diary data set, 3419 self-reported seizures were collected through a mobile application from 34 participants with epilepsy in Australia in 2018-2021. Daily average concentrations of carbon monoxide (CO), nitrogen dioxide (NO2 ), ozone (O3 ), particulate matter ≤10 µm in diameter (PM10 ), and sulfur dioxide (SO2 ) were retrieved from the Environment Protection Authority (EPA) based on participants' postcodes. A patient-time-stratified case-crossover design with the conditional Poisson regression model was used to determine the associations between air pollutants and epileptic seizures. RESULTS: A significant association between CO concentrations and epileptic seizure risks was observed, with an increased seizure risk of 4% (relative risk [RR]: 1.04, 95% confidence interval [CI]: 1.01-1.07) for an interquartile range (IQR) increase of CO concentrations (0.13 parts per million), whereas no significant associations were found for the other four air pollutants in the whole study population. Female participants had a significantly increased risk of seizures when exposed to elevated CO and NO2 , with RRs of 1.05 (95% CI: 1.01-1.08) and 1.09 (95% CI: 1.01-1.16), respectively. In addition, a significant association was observed between CO and the risk of subclinical seizures (RR: 1.20, 95% CI: 1.12-1.28). SIGNIFICANCE: Daily exposure to elevated CO concentrations may be associated with an increased risk of epileptic seizures, especially for subclinical seizures.

Learning receptive field properties of complex cells in V1.

There are two distinct classes of cells in the primary visual cortex (V1): simple cells and complex cells. One defining feature of complex cells is their spatial phase invariance; they respond strongly to oriented grating stimuli with a preferred orientation but with a wide range of spatial phases. A classical model of complete spatial phase invariance in complex cells is the energy model, in which the responses are the sum of the squared outputs of two linear spatially phase-shifted filters. However, recent experimental studies have shown that complex cells have a diverse range of spatial phase invariance and only a subset can be characterized by the energy model. While several models have been proposed to explain how complex cells could learn to be selective to orientation but invariant to spatial phase, most existing models overlook many biologically important details. We propose a biologically plausible model for complex cells that learns to pool inputs from simple cells based on the presentation of natural scene stimuli. The model is a three-layer network with rate-based neurons that describes the activities of LGN cells (layer 1), V1 simple cells (layer 2), and V1 complex cells (layer 3). The first two layers implement a recently proposed simple cell model that is biologically plausible and accounts for many experimental phenomena. The neural dynamics of the complex cells is modeled as the integration of simple cells inputs along with response normalization. Connections between LGN and simple cells are learned using Hebbian and anti-Hebbian plasticity. Connections between simple and complex cells are learned using a modified version of the Bienenstock, Cooper, and Munro (BCM) rule. Our results demonstrate that the learning rule can describe a diversity of complex cells, similar to those observed experimentally.

Electrical receptive fields of retinal ganglion cells: Influence of presynaptic neurons.

Implantable retinal stimulators activate surviving neurons to restore a sense of vision in people who have lost their photoreceptors through degenerative diseases. Complex spatial and temporal interactions occur in the retina during multi-electrode stimulation. Due to these complexities, most existing implants activate only a few electrodes at a time, limiting the repertoire of available stimulation patterns. Measuring the spatiotemporal interactions between electrodes and retinal cells, and incorporating them into a model may lead to improved stimulation algorithms that exploit the interactions. Here, we present a computational model that accurately predicts both the spatial and temporal nonlinear interactions of multi-electrode stimulation of rat retinal ganglion cells (RGCs). The model was verified using in vitro recordings of ON, OFF, and ON-OFF RGCs in response to subretinal multi-electrode stimulation with biphasic pulses at three stimulation frequencies (10, 20, 30 Hz). The model gives an estimate of each cell's spatiotemporal electrical receptive fields (ERFs); i.e., the pattern of stimulation leading to excitation or suppression in the neuron. All cells had excitatory ERFs and many also had suppressive sub-regions of their ERFs. We show that the nonlinearities in observed responses arise largely from activation of presynaptic interneurons. When synaptic transmission was blocked, the number of sub-regions of the ERF was reduced, usually to a single excitatory ERF. This suggests that direct cell activation can be modeled accurately by a one-dimensional model with linear interactions between electrodes, whereas indirect stimulation due to summated presynaptic responses is nonlinear.

Predictive coding of visual object position ahead of moving objects revealed by time-resolved EEG decoding.

Due to the delays inherent in neuronal transmission, our awareness of sensory events necessarily lags behind the occurrence of those events in the world. If the visual system did not compensate for these delays, we would consistently mislocalize moving objects behind their actual position. Anticipatory mechanisms that might compensate for these delays have been reported in animals, and such mechanisms have also been hypothesized to underlie perceptual effects in humans such as the Flash-Lag Effect. However, to date no direct physiological evidence for anticipatory mechanisms has been found in humans. Here, we apply multivariate pattern classification to time-resolved EEG data to investigate anticipatory coding of object position in humans. By comparing the time-course of neural position representation for objects in both random and predictable apparent motion, we isolated anticipatory mechanisms that could compensate for neural delays when motion trajectories were predictable. As well as revealing an early neural position representation (lag 80-90 ms) that was unaffected by the predictability of the object's trajectory, we demonstrate a second neural position representation at 140-150 ms that was distinct from the first, and that was pre-activated ahead of the moving object when it moved on a predictable trajectory. The latency advantage for predictable motion was approximately 16 ±â€¯2 ms. To our knowledge, this provides the first direct experimental neurophysiological evidence of anticipatory coding in human vision, revealing the time-course of predictive mechanisms without using a spatial proxy for time. The results are numerically consistent with earlier animal work, and suggest that current models of spatial predictive coding in visual cortex can be effectively extended into the temporal domain.

Learning Pitch with STDP: A Computational Model of Place and Temporal Pitch Perception Using Spiking Neural Networks.

Pitch perception is important for understanding speech prosody, music perception, recognizing tones in tonal languages, and perceiving speech in noisy environments. The two principal pitch perception theories consider the place of maximum neural excitation along the auditory nerve and the temporal pattern of the auditory neurons' action potentials (spikes) as pitch cues. This paper describes a biophysical mechanism by which fine-structure temporal information can be extracted from the spikes generated at the auditory periphery. Deriving meaningful pitch-related information from spike times requires neural structures specialized in capturing synchronous or correlated activity from amongst neural events. The emergence of such pitch-processing neural mechanisms is described through a computational model of auditory processing. Simulation results show that a correlation-based, unsupervised, spike-based form of Hebbian learning can explain the development of neural structures required for recognizing the pitch of simple and complex tones, with or without the fundamental frequency. The temporal code is robust to variations in the spectral shape of the signal and thus can explain the phenomenon of pitch constancy.

Single-compartment models of retinal ganglion cells with different electrophysiologies.

There are more than 15 different types of retinal ganglion cells (RGCs) in the mammalian retina. To model responses of RGCs to electrical stimulation, we use single-compartment Hodgkin-Huxley-type models and run simulations in the Neuron environment. We use our recently published in vitro data of different morphological cell types to constrain the model, and study the effects of electrophysiology on the cell responses separately from the effects of morphology. We find simple models that can match the spike patterns of different types of RGCs. These models, with different input-output properties, may be used in a network to study retinal network dynamics and interactions.

Spike history neural response model.

There is a potential for improved efficacy of neural stimulation if stimulation levels can be modified dynamically based on the responses of neural tissue in real time. A neural model is developed that describes the response of neurons to electrical stimulation and that is suitable for feedback control neuroprosthetic stimulation. Experimental data from NZ white rabbit retinae is used with a data-driven technique to model neural dynamics. The linear-nonlinear approach is adapted to incorporate spike history and to predict the neural response of ganglion cells to electrical stimulation. To validate the fitness of the model, the penalty term is calculated based on the time difference between each simulated spike and the closest spike in time in the experimentally recorded train. The proposed model is able to robustly predict experimentally observed spike trains.

Interplay of intrinsic and synaptic conductances in the generation of high-frequency oscillations in interneuronal networks with irregular spiking.

High-frequency oscillations (above 30 Hz) have been observed in sensory and higher-order brain areas, and are believed to constitute a general hallmark of functional neuronal activation. Fast inhibition in interneuronal networks has been suggested as a general mechanism for the generation of high-frequency oscillations. Certain classes of interneurons exhibit subthreshold oscillations, but the effect of this intrinsic neuronal property on the population rhythm is not completely understood. We study the influence of intrinsic damped subthreshold oscillations in the emergence of collective high-frequency oscillations, and elucidate the dynamical mechanisms that underlie this phenomenon. We simulate neuronal networks composed of either Integrate-and-Fire (IF) or Generalized Integrate-and-Fire (GIF) neurons. The IF model displays purely passive subthreshold dynamics, while the GIF model exhibits subthreshold damped oscillations. Individual neurons receive inhibitory synaptic currents mediated by spiking activity in their neighbors as well as noisy synaptic bombardment, and fire irregularly at a lower rate than population frequency. We identify three factors that affect the influence of single-neuron properties on synchronization mediated by inhibition: i) the firing rate response to the noisy background input, ii) the membrane potential distribution, and iii) the shape of Inhibitory Post-Synaptic Potentials (IPSPs). For hyperpolarizing inhibition, the GIF IPSP profile (factor iii)) exhibits post-inhibitory rebound, which induces a coherent spike-mediated depolarization across cells that greatly facilitates synchronous oscillations. This effect dominates the network dynamics, hence GIF networks display stronger oscillations than IF networks. However, the restorative current in the GIF neuron lowers firing rates and narrows the membrane potential distribution (factors i) and ii), respectively), which tend to decrease synchrony. If inhibition is shunting instead of hyperpolarizing, post-inhibitory rebound is not elicited and factors i) and ii) dominate, yielding lower synchrony in GIF networks than in IF networks.

The effect of morphology upon electrophysiological responses of retinal ganglion cells: simulation results.

Retinal ganglion cells (RGCs) display differences in their morphology and intrinsic electrophysiology. The goal of this study is to characterize the ionic currents that explain the behavior of ON and OFF RGCs and to explore if all morphological types of RGCs exhibit the phenomena described in electrophysiological data. We extend our previous single compartment cell models of ON and OFF RGCs to more biophysically realistic multicompartment cell models and investigate the effect of cell morphology on intrinsic electrophysiological properties. The membrane dynamics are described using the Hodgkin - Huxley type formalism. A subset of published patch-clamp data from isolated intact mouse retina is used to constrain the model and another subset is used to validate the model. Two hundred morphologically distinct ON and OFF RGCs are simulated with various densities of ionic currents in different morphological neuron compartments. Our model predicts that the differences between ON and OFF cells are explained by the presence of the low voltage activated calcium current in OFF cells and absence of such in ON cells. Our study shows through simulation that particular morphological types of RGCs are capable of exhibiting the full range of phenomena described in recent experiments. Comparisons of outputs from different cells indicate that the RGC morphologies that best describe recent experimental results are ones that have a larger ratio of soma to total surface area.

Delay selection by spike-timing-dependent plasticity in recurrent networks of spiking neurons receiving oscillatory inputs.

Learning rules, such as spike-timing-dependent plasticity (STDP), change the structure of networks of neurons based on the firing activity. A network level understanding of these mechanisms can help infer how the brain learns patterns and processes information. Previous studies have shown that STDP selectively potentiates feed-forward connections that have specific axonal delays, and that this underlies behavioral functions such as sound localization in the auditory brainstem of the barn owl. In this study, we investigate how STDP leads to the selective potentiation of recurrent connections with different axonal and dendritic delays during oscillatory activity. We develop analytical models of learning with additive STDP in recurrent networks driven by oscillatory inputs, and support the results using simulations with leaky integrate-and-fire neurons. Our results show selective potentiation of connections with specific axonal delays, which depended on the input frequency. In addition, we demonstrate how this can lead to a network becoming selective in the amplitude of its oscillatory response to this frequency. We extend this model of axonal delay selection within a single recurrent network in two ways. First, we show the selective potentiation of connections with a range of both axonal and dendritic delays. Second, we show axonal delay selection between multiple groups receiving out-of-phase, oscillatory inputs. We discuss the application of these models to the formation and activation of neuronal ensembles or cell assemblies in the cortex, and also to missing fundamental pitch perception in the auditory brainstem.

Multi-frequency steady-state visual evoked potential dataset.

The Steady-State Visual Evoked Potential (SSVEP) is a widely used modality in Brain-Computer Interfaces (BCIs). Existing research has demonstrated the capabilities of SSVEP that use single frequencies for each target in various applications with relatively small numbers of commands required in the BCI. Multi-frequency SSVEP has been developed to extend the capability of single-frequency SSVEP to tasks that involve large numbers of commands. However, the development on multi-frequency SSVEP methodologies is falling behind compared to the number of studies with single-frequency SSVEP. This dataset was constructed to promote research in multi-frequency SSVEP by making SSVEP signals collected with different frequency stimulation settings publicly available. In this dataset, SSVEPs were collected from 35 participants using single-, dual-, and tri-frequency stimulation and with three different multi-frequency stimulation variants.

Understanding visual processing of motion: completing the picture using experimentally driven computational models of MT.

Computational modeling helps neuroscientists to integrate and explain experimental data obtained through neurophysiological and anatomical studies, thus providing a mechanism by which we can better understand and predict the principles of neural computation. Computational modeling of the neuronal pathways of the visual cortex has been successful in developing theories of biological motion processing. This review describes a range of computational models that have been inspired by neurophysiological experiments. Theories of local motion integration and pattern motion processing are presented, together with suggested neurophysiological experiments designed to test those hypotheses.

Spectral analysis of input spike trains by spike-timing-dependent plasticity.

Spike-timing-dependent plasticity (STDP) has been observed in many brain areas such as sensory cortices, where it is hypothesized to structure synaptic connections between neurons. Previous studies have demonstrated how STDP can capture spiking information at short timescales using specific input configurations, such as coincident spiking, spike patterns and oscillatory spike trains. However, the corresponding computation in the case of arbitrary input signals is still unclear. This paper provides an overarching picture of the algorithm inherent to STDP, tying together many previous results for commonly used models of pairwise STDP. For a single neuron with plastic excitatory synapses, we show how STDP performs a spectral analysis on the temporal cross-correlograms between its afferent spike trains. The postsynaptic responses and STDP learning window determine kernel functions that specify how the neuron "sees" the input correlations. We thus denote this unsupervised learning scheme as 'kernel spectral component analysis' (kSCA). In particular, the whole input correlation structure must be considered since all plastic synapses compete with each other. We find that kSCA is enhanced when weight-dependent STDP induces gradual synaptic competition. For a spiking neuron with a "linear" response and pairwise STDP alone, we find that kSCA resembles principal component analysis (PCA). However, plain STDP does not isolate correlation sources in general, e.g., when they are mixed among the input spike trains. In other words, it does not perform independent component analysis (ICA). Tuning the neuron to a single correlation source can be achieved when STDP is paired with a homeostatic mechanism that reinforces the competition between synaptic inputs. Our results suggest that neuronal networks equipped with STDP can process signals encoded in the transient spiking activity at the timescales of tens of milliseconds for usual STDP.

Quantifying visual acuity for pre-clinical testing of visual prostheses.

Objective.Visual prostheses currently restore only limited vision. More research and pre-clinical work are required to improve the devices and stimulation strategies that are used to induce neural activity that results in visual perception. Evaluation of candidate strategies and devices requires an objective way to convert measured and modelled patterns of neural activity into a quantitative measure of visual acuity.Approach.This study presents an approach that compares evoked patterns of neural activation with target and reference patterns. A d-prime measure of discriminability determines whether the evoked neural activation pattern is sufficient to discriminate between the target and reference patterns and thus provides a quantified level of visual perception in the clinical Snellen and MAR scales. The magnitude of the resulting value was demonstrated using scaled standardized 'C' and 'E' optotypes.Main results.The approach was used to assess the visual acuity provided by two alternative stimulation strategies applied to simulated retinal implants with different electrode pitch configurations and differently sized spreads of neural activity. It was found that when there is substantial overlap in neural activity generated by different electrodes, an estimate of acuity based only upon electrode pitch is incorrect; our proposed method gives an accurate result in both circumstances.Significance.Quantification of visual acuity using this approach in pre-clinical development will allow for more rapid and accurate prototyping of improved devices and neural stimulation strategies.

Effect of alpha range activity on SSVEP decoding in brain-computer interfaces.

Brain-computer interfaces (BCIs) facilitate direct communication between the brain and external devices. For BCI technology to be commercialized for wide scale applications, BCIs should be accurate, efficient, and exhibit consistency in performance for a wide variety of users. A core challenge is the physiological and anatomical differences amongst people, which causes a high variability amongst participants in BCI studies. Hence, it becomes necessary to analyze the mechanisms causing this variability and address them by improving the decoding algorithms. In this paper, a publicly available steady-state visual evoked potential (SSVEP) dataset is analyzed to study the effect of SSVEP flicker on the endogenous alpha power and the subsequent overall effect on the classification accuracy of the participants. It was observed that the participants with classification accuracy below 95% showed increased alpha power in their brain activities. Incorrect prediction in the decoding algorithm was observed a maximum number of times when the predicted frequency was in the range 9-12 Hz. We conclude that frequencies between 9-12 Hz may result in below par performance in some participants when canonical correlation analysis is used for classification.Clinical relevance-If alpha-band frequencies are used for SSVEP stimulation, alpha power interference in EEG may alter BCI accuracy for some users.

Critical dynamics arise during structured information presentation within embodied in vitro neuronal networks.

Understanding how brains process information is an incredibly difficult task. Amongst the metrics characterising information processing in the brain, observations of dynamic near-critical states have generated significant interest. However, theoretical and experimental limitations associated with human and animal models have precluded a definite answer about when and why neural criticality arises with links from attention, to cognition, and even to consciousness. To explore this topic, we used an in vitro neural network of cortical neurons that was trained to play a simplified game of 'Pong' to demonstrate Synthetic Biological Intelligence (SBI). We demonstrate that critical dynamics emerge when neural networks receive task-related structured sensory input, reorganizing the system to a near-critical state. Additionally, better task performance correlated with proximity to critical dynamics. However, criticality alone is insufficient for a neuronal network to demonstrate learning in the absence of additional information regarding the consequences of previous actions. These findings offer compelling support that neural criticality arises as a base feature of incoming structured information processing without the need for higher order cognition.

Inhibitory stabilized network behaviour in a balanced neural mass model of a cortical column.

Strong inhibitory recurrent connections can reduce the tendency for a neural network to become unstable. This is known as inhibitory stabilization; networks that are unstable in the absence of strong inhibitory feedback because of their unstable excitatory recurrent connections are known as Inhibition Stabilized Networks (ISNs). One of the characteristics of ISNs is their "paradoxical response", where perturbing the inhibitory neurons with additional excitatory input results in a decrease in their activity after a temporal delay instead of increasing their activity. Here, we develop a model of populations of neurons across different layers of cortex. Within each layer, there is one population of inhibitory neurons and one population of excitatory neurons. The connectivity weights across different populations in the model are derived from a synaptic physiology database provided by the Allen Institute. The model shows a gradient of excitation-inhibition balance across different layers in the cortex, where superficial layers are more inhibitory dominated compared to deeper layers. To investigate the presence of ISNs across different layers, we measured the membrane potentials of neural populations in the model after perturbing inhibitory populations. The results show that layer 2/3 in the model does not operate in the ISN regime but layers 4 and 5 do operate in the ISN regime. These results accord with neurophysiological findings that explored the presence of ISNs across different layers in the cortex. The results show that there may be a systematic macroscopic gradient of inhibitory stabilization across different layers in the cortex that depends on the level of excitation-inhibition balance, and that the strength of the paradoxical response increases as the model moves closer to bifurcation points.