94 research outputs found

    A BIOLOGICAL BASED MODEL OF THE HUMAN VISUAL SYSTEM INCORPORATING LATERAL SUBTRACTIVE INHIBITION WITH NON-UNIFORM SAMPLING AND MULTIPLE SPATIAL FREQUENCY FILTERS

    Get PDF
    The human visual system has been an interesting topic of scientific research for decades. It is known that the cone photo-receptors are arrayed in a non-linear fashion and that a lateral subtractive inhibitory process is occurring in the visual pathway. This thesis outlines for the first time how lateral subtractive inhibition manifests itself in the context of a non-uniform sensor distribution where the distance between cone photo-receptors, and size of the receptors, are varying in a log manner when moving radially away from the foveal area. Range limits on the parameters that control the non-uniform sampling and coupling coefficients are presented and optimal values are identified for specific image resolutions. The results of this analysis are then coupled to a proposed model of spatial frequency filtering to assist in subsequent studies of feature extraction and pattern analysis. The filters generated are based on three spatial-frequency channels that are designed to model the human eye contrast sensitivity curve. Simulated results are presented

    Membrane resistance and shunting inhibition: where biophysics meets state-dependent human neurophysiology

    Get PDF
    Activation of neurons not only changes their membrane potential and firing rate but, as a secondary action reduces membrane resistance. This loss of resistance, or increase of conductance, may be of central importance in non-invasive magnetic or electric stimulation of the human brain since electrical fields cause larger changes in transmembrane voltage in resting neurones with low membrane conductances than in active neurones with high conductance. This may explain why both the immediate and after-effects of brain stimulation are smaller or even reversed during voluntary activity compared to rest. Membrane conductance is also increased during shunting inhibition, which accompanies the classic GABAa IPSP. This short-circuits nearby EPSPs and is suggested here to contribute to the magnitude and time course of short latency intracortical inhibition (SICI) and facilitation (ICF). This article is protected by copyright. All rights reserved

    A Neural Network Model for the Spatial and Temporal Response of Retinal Ganglion Cells

    Full text link
    This article introduces a quantitative model of early visual system function. The model is formulated to unify analyses of spatial and temporal information processing by the nervous system. Functional constraints of the model suggest mechanisms analogous to photoreceptors, bipolar cells, and retinal ganglion cells, which can be formally represented with first order differential equations. Preliminary numerical simulations and analytical results show that the same formal mechanisms can explain the behavior of both X (linear) and Y (nonlinear) retinal ganglion cell classes by simple changes in the relative width of the receptive field (RF) center and surround mechanisms. Specifically, an increase in the width of the RF center results in a change from X-like to Y-like response, in agreement with anatomical data on the relationship between α- and -cell RF profiles. Simulations of model response to various spatio-temporal input patterns replicate many of the classical properties of X and Y cells, including transient (Y) versus sustained (X) responses, null-phase responses to alternating gratings in X cells, on-off or frequency doubling responses in Y cells, and phase-independent on-off responses in Y cells at high spatial frequencies. The model's formal mechanisms may be used in other portions of the visual system and more generally in nervous system structures involved with spatio-temporal information processing

    Modeling biophysical and neural circuit bases for core cognitive abilities evident in neuroimaging patterns: hippocampal mismatch, mismatch negativity, repetition positivity, and alpha suppression of distractors

    Get PDF
    This dissertation develops computational models to address outstanding problems in the domain of expectation-related cognitive processes and their neuroimaging markers in functional MRI or EEG. The new models reveal a way to unite diverse phenomena within a common framework focused on dynamic neural encoding shifts, which can arise from robust interactive effects of M-currents and chloride currents in pyramidal neurons. By specifying efficient, biologically realistic circuits that achieve predictive coding (e.g., Friston, 2005), these models bridge among neuronal biophysics, systems neuroscience, and theories of cognition. Chapter one surveys data types and neural processes to be examined, and outlines the Dynamically Labeled Predictive Coding (DLPC) framework developed during the research. Chapter two models hippocampal prediction and mismatch, using the DLPC framework. Chapter three presents extensions to the model that allow its application for modeling neocortical EEG genesis. Simulations of this extended model illustrate how dynamic encoding shifts can produce Mismatch Negativity (MMN) phenomena, including pharmacological effects on MMN reported for humans or animals. Chapters four and five describe new modeling studies of possible neural bases for alpha-induced information suppression, a phenomenon associated with active ignoring of stimuli. Two models explore the hypothesis that in simple rate-based circuits, information suppression might be a robust effect of neural saturation states arising near peaks of resonant alpha oscillations. A new proposal is also introduced for how the basal ganglia may control onset and offset of alpha-induced information suppression. Although these rate models could reproduce many experimental findings, they fell short of reproducing a key electrophysiological finding: phase-dependent reduction in spiking activity correlated with power in the alpha frequency band. Therefore, chapter five also specifies how a DLPC model, adapted from the neocortical model developed in chapter three, can provide an expectation-based model of alpha-induced information suppression that exhibits phase-dependent spike reduction during alpha-band oscillations. The model thus can explain experimental findings that were not reproduced by the rate models. The final chapter summarizes main theses, results, and basic research implications, then suggests future directions, including expanded models of neocortical mismatch, applications to artificial neural networks, and the introduction of reward circuitry

    Investigating the role of fast-spiking interneurons in neocortical dynamics

    Get PDF
    PhD ThesisFast-spiking interneurons are the largest interneuronal population in neocortex. It is well documented that this population is crucial in many functions of the neocortex by subserving all aspects of neural computation, like gain control, and by enabling dynamic phenomena, like the generation of high frequency oscillations. Fast-spiking interneurons, which represent mainly the parvalbumin-expressing, soma-targeting basket cells, are also implicated in pathological dynamics, like the propagation of seizures or the impaired coordination of activity in schizophrenia. In the present thesis, I investigate the role of fast-spiking interneurons in such dynamic phenomena by using computational and experimental techniques. First, I introduce a neural mass model of the neocortical microcircuit featuring divisive inhibition, a gain control mechanism, which is thought to be delivered mainly by the soma-targeting interneurons. Its dynamics were analysed at the onset of chaos and during the phenomena of entrainment and long-range synchronization. It is demonstrated that the mechanism of divisive inhibition reduces the sensitivity of the network to parameter changes and enhances the stability and exibility of oscillations. Next, in vitro electrophysiology was used to investigate the propagation of activity in the network of electrically coupled fast-spiking interneurons. Experimental evidence suggests that these interneurons and their gap junctions are involved in the propagation of seizures. Using multi-electrode array recordings and optogenetics, I investigated the possibility of such propagating activity under the conditions of raised extracellular K+ concentration which applies during seizures. Propagated activity was recorded and the involvement of gap junctions was con rmed by pharmacological manipulations. Finally, the interaction between two oscillations was investigated. Two oscillations with di erent frequencies were induced in cortical slices by directly activating the pyramidal cells using optogenetics. Their interaction suggested the possibility of a coincidence detection mechanism at the circuit level. Pharmacological manipulations were used to explore the role of the inhibitory interneurons during this phenomenon. The results, however, showed that the observed phenomenon was not a result of synaptic activity. Nevertheless, the experiments provided some insights about the excitability of the tissue through scattered light while using optogenetics. This investigation provides new insights into the role of fast-spiking interneurons in the neocortex. In particular, it is suggested that the gain control mechanism is important for the physiological oscillatory dynamics of the network and that the gap junctions between these interneurons can potentially contribute to the inhibitory restraint during a seizure.Wellcome Trust

    A Nonlinear Model of Spatiotemporal Retinal Processing: Simulations of X and Y Retinal Ganglion Cell Behavior

    Full text link
    This article describes a nonlinear model of neural processing in the vertebrate retina, comprising model photoreceptors, model push-pull bipolar cells, and model ganglion cells. Previous analyses and simulations have shown that with a choice of parameters that mimics beta cells, the model exhibits X-like linear spatial summation (null response to contrast-reversed gratings) in spite of photoreceptor nonlinearities; on the other hand, a choice of parameters that mimics alpha cells leads to Y-like frequency doubling. This article extends the previous work by showing that the model can replicate qualitatively many of the original findings on X and Y cells with a fixed choice of parameters. The results generally support the hypothesis that X and Y cells can be seen as functional variants of a single neural circuit. The model also suggests that both depolarizing and hyperpolarizing bipolar cells converge onto both ON and OFF ganglion cell types. The push-pull connectivity enables ganglion cells to remain sensitive to deviations about the mean output level of nonlinear photoreceptors. These and other properties of the push-pull model are discussed in the general context of retinal processing of spatiotemporal luminance patterns.Alfred P. Sloan Research Fellowship (BR-3122); Air Force Office of Scientific Research (F49620-92-J-0499

    Computational Properties of Cerebellar Nucleus Neurons: Effects of Stochastic Ion Channel Gating and Input Location

    Get PDF
    The function of the nervous system is shaped by the refined integration of synaptic inputs taking place at the single neuron level. Gain modulation is a computational principle that is widely used across the brain, in which the response of a neuronal unit to a set of inputs is affected in a multiplicative fashion by a second set of inputs, but without any effect on its selectivity. The arithmetic operations performed by pyramidal cells in cortical brain areas have been well characterised, along with the underlying mechanisms at the level of networks and cells, for instance background synaptic noise and dendritic saturation. However, in spite of the vast amount of research on the cerebellum and its function, little is known about neuronal computations carried out by its cellular components. A particular area of interest are the cerebellar nuclei, the main output gate of the cerebellum to the brain stem and cortical areas. The aim of this thesis is to contribute to an understanding of the arithmetic operations performed by neurons in the cerebellar nuclei. Focus is placed on two putative determinants, the location of the synaptic input and the presence of channel noise. To analyse the effect of channel noise, the known voltage-gated ion channels of a cerebellar nucleus neuron model are translated to stochastic Markov formalisms and their electrophysiologial behaviour is compared to their deterministic Hodgkin-Huxley counterparts. The findings demonstrate that in most cases, the behaviour of stochastic channels matches the reference deterministic models, with the notable exception of voltage-gated channels with fast kinetics. Two potential explanations are suggested for this discrepancy. Firstly, channels with fast kinetics are strongly affected by the artefactual loss of gating events in the simulation that is caused by the use of a finite-length time step. While this effect can be mitigated, in part, by using very small time steps, the second source of simulation artefacts is the rectification of the distribution of open channels, when channel kinetics characteristics allow the generation of a window current, with an temporal-averaged equilibrium close to zero. Further, stochastic gating is implemented in a realistic cerebellar nucleus neuronal model. The resulting stochastic model exhibits probabilistic spiking and a similar output rate as the corresponding deterministic cerebellar nucleus neuronal model. However, the outcomes of this thesis indicate the computational properties of the cerebellar nucleus neuronal model are independent of the presence of ion channel noise. The main result of this thesis is that the synaptic input location determines the single neuron computational properties, both in the cerebellar nucleus and layer Vb pyramidal neuronal models. The extent of multiplication increases systematically with the distance from the soma, for the cerebellar nucleus, but not for the layer Vb pyramidal neuron, where it is smaller than it would be expected for the distance from the soma. For both neurons, the underlying mechanism is related to the combined effect of nonlinearities introduced by dendritic saturation and the synaptic input noise. However, while excitatory inputs in the perisomatic areas in the cerebellar nucleus undergo additive operations and the distal areas multiplicative, in the layer Vb pyramidal neuron the integration of the excitatory driving input is always multiplicative. In addition, the change in gain is sensitive to the synchronicity of the excitatory synaptic input in the layer Vb pyramidal neuron, but not in the cerebellar nucleus neuron. These observations indicate that the same gain control mechanism might be utilized in distinct ways, in different computational contexts and across different areas, based on the neuronal type and its function

    Response-dependent dynamics of cell-specific inhibition in cortical networks in vivo

    Get PDF
    In the visual cortex, inhibitory neurons alter the computations performed by target cells via combination of two fundamental operations, division and subtraction. The origins of these operations have been variously ascribed to differences in neuron classes, synapse location or receptor conductances. Here, by utilizing specific visual stimuli and single optogenetic probe pulses, we show that the function of ​parvalbumin-expressing and ​somatostatin-expressing neurons in mice in vivo is governed by the overlap of response timing between these neurons and their targets. In particular, ​somatostatin-expressing neurons respond at longer latencies to small visual stimuli compared with their target neurons and provide subtractive inhibition. With large visual stimuli, however, they respond at short latencies coincident with their target cells and switch to provide divisive inhibition. These results indicate that inhibition mediated by these neurons is a dynamic property of cortical circuits rather than an immutable property of neuronal classes.Marie Curie International Fellowship (Postdoctoral Fellowship FP7-PEOPLE-2010-IOF))National Institutes of Health (U.S.) (Grant EY007023)National Institutes of Health (U.S.) (Grant NS090473)Simons Foundatio
    • …
    corecore