Journal of Computational Neuroscience最新文献

Central pattern generators are characterized by a heterogeneous cellular composition, with different cell types playing distinct roles in the production and transmission of rhythmic signals. However, little is known about the functional implications of individual variation in the relative distributions of cells and their connectivity patterns. Here, we addressed this question through a combination of morphological data analysis and computational modeling, using the pacemaker nucleus of the weakly electric fish Apteronotus leptorhynchus as case study. A neural network comprised of 60-110 interconnected pacemaker cells and 15-30 relay cells conveying its output to electromotoneurons in the spinal cord, this nucleus continuously generates neural signals at frequencies of up to 1 kHz with high temporal precision. We systematically explored the impact of network size and density on oscillation frequencies and their variation within and across cells. To accurately determine effect sizes, we minimized the likelihood of complex dynamics using a simplified setup precluding differential delays. To identify natural constraints, parameter ranges were extended beyond experimentally recorded numbers of cells and connections. Simulations revealed that pacemaker cells have higher frequencies and lower within-population variability than relay cells. Within-cell precision and between-cells frequency synchronization increased with the number of pacemaker cells and of connections of either type, and decreased with relay cell count in both populations. Network-level frequency-synchronized oscillations occurred in roughly half of simulations, with maximized likelihood and firing precision within biologically observed parameter ranges. These findings suggest the structure of the biological pacemaker nucleus is optimized for generating synchronized sustained oscillations.

Between the onset of the critical period of mouse primary visual cortex and eye opening at postnatal day 14 is a complex process and that is vital for the cognitive function of vision. The onset of the critical period of mouse primary visual cortex involves changes of the intrinsic firing property of each neuron and short term plasticity of synapses. In order to investigate the functional role of each factor in regulating the circuit firing activity during the critical period plasticity, we adopted the Markram's model for short term plasticity and Wilson's model for intrinsic neuron firing activity, and construct a microcircuit for mouse visual cortex layer IV based on the connection probabilities from experimental results. Our results indicate that, during CP development, the most critical factors that regulate the firing pattern of microcircuit is the short term plasticity of the synapse from PC to PV and SST interneurons, which upregulates the PV interneuron firing and produces new balance between excitation and inhibition; the intrinsic firing activity of PC and PV during development downregulates the firing frequency of the circuits. In addition, we have investigated the function of feedforward excitatory thalamic-cortical projection to PC and PV interneuron during CP, and found that neural firing activity largely depends on the TC input and the results are similar to the local circuit with minor differences. We conclude that the short term plasticity development during critical period plays a crucial role in regulating the circuit behavior.

Using the improved memristive Izhikevich neuron model, the effects of autaptic connection as well as electromagnetic induction are studied on the dynamical behavior of neuronal spiking. Using bifurcation analysis for membrane potentials, the effects of autaptic and electromagnetic parameters on the mode transition in electrical activities of the neuron model are investigated. Furthermore, white Gaussian noise is considered in the neuron model, to evaluate the effect of electromagnetic disturbance on the firing pattern of the neuron using the coefficient of variation. The bifurcation diagram versus autaptic conductance and time delay has been extensively studied. The results show that the effects of autaptic connection as well as electromagnetic induction on the spiking behavior of neurons can be well demonstrated by using the Izhikevich model. The electrical activities of the Izhikevich neuron model become more complex when the effects of autaptic connection and electromagnetic induction are considered in the neuron model. Using the Izhikevich neuron model, the high variety of spiking/bursting patterns is represented in the bifurcation diagram of inter-spike interval versus autaptic or electromagnetic parameters. Noise can have distinct effects on the spiking activity of the neuron, for the subthreshold input current, increasing the intensity of the electromagnetic noise increases the regularity of the neuron spiking, but for the suprathreshold input current, the regularity of spiking decreases with noise.

Place cells develop spatially-tuned receptive fields during the early stages of novel environment exploration. The generative mechanism underlying these spatially-selective responses remains largely elusive, but has been associated with theta rhythmicity. An important factor implicating the transformation of silent cells to place cells is a spatially-uniform depolarization that is mediated by a persistent sodium current. This neuronal current is modulated by extracellular calcium concentration, which, in turn, is actively controlled by astrocytes. However, there is no established relationship between the neuronal depolarization and astrocytic activity. To consider this link, we designed a bioplausible computational model of a neuronal-astrocytic network, where astrocytes induced the transient emergence of place fields in silent cells, and accelerated the plasticity-induced consolidation of place cells. Interestingly, theta oscillations emerged naturally at the network level, resulting from the astrocytic modulation of subcellular neuronal properties. Our results suggest that astrocytes participate in spatial mapping and exploration, and further highlight the computational roles of these cells in the brain.

The mechanisms underlying the generation of hippocampal epileptic seizures and interictal events and their interactions with the sleep-wake cycle are not yet fully understood. Indeed, medial temporal lobe epilepsy is associated with hippocampal abnormalities both at the neuronal (channelopathies, impaired potassium and chloride dynamics) and network level (neuronal and axonal loss, mossy fiber sprouting), with more frequent seizures during wakefulness compared with slow-wave sleep. In this article, starting from our previous computational modeling work of the hippocampal formation based on realistic topology and synaptic connectivity, we study the role of micro- and mesoscale pathological conditions of the epileptic hippocampus in the generation and maintenance of seizure-like theta and interictal oscillations. We show, through the simulations of hippocampal activity during slow-wave sleep and wakefulness that: (i) both mossy fiber sprouting and sclerosis account for seizure-like theta activity, (ii) but they have antagonist effects (seizure-like activity occurrence increases with sprouting but decreases with sclerosis), (iii) though impaired potassium and chloride dynamics have little influence on the generation of seizure-like activity, they do play a role on the generation of interictal patterns, and (iv) seizure-like activity and fast ripples are more likely to occur during wakefulness and interictal spikes during sleep.

An important function of the brain is to predict which stimulus is likely to occur based on the perceived cues. The present research studied the branching behavior of a computational network model of populations of excitatory and inhibitory neurons, both analytically and through simulations. Results show how synaptic efficacy, retroactive inhibition and short-term synaptic depression determine the dynamics of selection between different branches predicting sequences of stimuli of different probabilities. Further results show that changes in the probability of the different predictions depend on variations of neuronal gain. Such variations allow the network to optimize the probability of its predictions to changing probabilities of the sequences without changing synaptic efficacy.

Temporal filters, the ability of postsynaptic neurons to preferentially select certain presynaptic input patterns over others, have been shown to be associated with the notion of information filtering and coding of sensory inputs. Short-term plasticity (depression and facilitation; STP) has been proposed to be an important player in the generation of temporal filters. We carry out a systematic modeling, analysis and computational study to understand how characteristic postsynaptic (low-, high- and band-pass) temporal filters are generated in response to periodic presynaptic spike trains in the presence STP. We investigate how the dynamic properties of these filters depend on the interplay of a hierarchy of processes, including the arrival of the presynaptic spikes, the activation of STP, its effect on the excitatory synaptic connection efficacy, and the response of the postsynaptic cell. These mechanisms involve the interplay of a collection of time scales that operate at the single-event level (roughly, during each presynaptic interspike-interval) and control the long-term development of the temporal filters over multiple presynaptic events. These time scales are generated at the levels of the presynaptic cell (captured by the presynaptic interspike-intervals), short-term depression and facilitation, synaptic dynamics and the post-synaptic cellular currents. We develop mathematical tools to link the single-event time scales with the time scales governing the long-term dynamics of the resulting temporal filters for a relatively simple model where depression and facilitation interact at the level of the synaptic efficacy change. We extend our results and tools to account for more complex models. These include multiple STP time scales and non-periodic presynaptic inputs. The results and ideas we develop have implications for the understanding of the generation of temporal filters in complex networks for which the simple feedforward network we investigate here is a building block.

Models of synaptic plasticity have been used to better understand neural development as well as learning and memory. One prominent classic model is the Bienenstock-Cooper-Munro (BCM) model that has been particularly successful in explaining plasticity of the visual cortex. Here, in an effort to include more biophysical detail in the BCM model, we incorporate 1) feedforward inhibition, and 2) the experimental observation that large synapses are relatively harder to potentiate than weak ones, while synaptic depression is proportional to the synaptic strength. These modifications change the outcome of unsupervised plasticity under the BCM model. The amount of feed-forward inhibition adds a parameter to BCM that turns out to determine the strength of competition. In the limit of strong inhibition the learning outcome is identical to standard BCM and the neuron becomes selective to one stimulus only (winner-take-all). For smaller values of inhibition, competition is weaker and the receptive fields are less selective. However, both BCM variants can yield realistic receptive fields.