Journal of Computational Neuroscience最新文献

Traumatic brain injury (TBI) can have a multitude of effects on neural functioning. In extreme cases, TBI can lead to seizures both immediately following the injury as well as persistent epilepsy over years to a lifetime. However, mechanisms of neural dysfunctioning after TBI remain poorly understood. To address these questions, we analyzed human and animal data and we developed a biophysical network model implementing effects of ion concentration dynamics and homeostatic synaptic plasticity to test effects of TBI on the brain network dynamics. We focus on three primary phenomena that have been reported in vivo after TBI: an increase in infra slow oscillations (<0.1 Hz), increase in Delta power (1 - 4 Hz), and the emergence of broadband Gamma bursts (30 - 100 Hz). Using computational network model, we show that the infra slow oscillations can be directly attributed to extracellular potassium dynamics, while the increase in Delta power and occurrence of Gamma bursts are related to the increase in strength of synaptic weights from homeostatic synaptic scaling triggered by trauma. We also show that the buildup of Gamma bursts in the injured region can lead to seizure-like events that propagate across the entire network; seizures can then be initiated in previously healthy regions. This study brings greater understanding of the network effects of TBI and how they can lead to epileptic activity. This lays the foundation to begin investigating how injured networks can be healed and seizures prevented.

Firing rate models for describing the mean-field activities of neuronal ensembles can be used effectively to study network function and dynamics, including synchronization and rhythmicity of excitatory-inhibitory populations. However, traditional Wilson-Cowan-like models, even when extended to include an explicit dynamic synaptic activation variable, are found unable to capture some dynamics such as Interneuronal Network Gamma oscillations (ING). Use of an explicit delay is helpful in simulations at the expense of complicating mathematical analysis. We resolve this issue by introducing a dynamic variable, u, that acts as an effective delay in the negative feedback loop between firing rate (r) and synaptic gating of inhibition (s). In effect, u endows synaptic activation with second order dynamics. With linear stability analysis, numerical branch-tracking and simulations, we show that our r-u-s rate model captures some key qualitative features of spiking network models for ING. We also propose an alternative formulation, a v-u-s model, in which mean membrane potential v satisfies an averaged current-balance equation. Furthermore, we extend the framework to E-I networks. With our six-variable v-u-s model, we demonstrate in firing rate models the transition from Pyramidal-Interneuronal Network Gamma (PING) to ING by increasing the external drive to the inhibitory population without adjusting synaptic weights. Having PING and ING available in a single network, without invoking synaptic blockers, is plausible and natural for explaining the emergence and transition of two different types of gamma oscillations.

We characterise cortical dynamics using partial differential equations (PDEs), analysing various connectivity patterns within the cortical sheet. This exploration yields diverse dynamics, encompassing wave equations and limit cycle activity. We presume balanced equations between excitatory and inhibitory neuronal units, reflecting the ubiquitous oscillatory patterns observed in electrophysiological measurements. Our derived dynamics comprise lowest-order wave equations (i.e., the Klein-Gordon model), limit cycle waves, higher-order PDE formulations, and transitions between limit cycles and near-zero states. Furthermore, we delve into the symmetries of the models using the Lagrangian formalism, distinguishing between continuous and discontinuous symmetries. These symmetries allow for mathematical expediency in the analysis of the model and could also be useful in studying the effect of symmetrical input from distributed cortical regions. Overall, our ability to derive multiple constraints on the fields - and predictions of the model - stems largely from the underlying assumption that the brain operates at a critical state. This assumption, in turn, drives the dynamics towards oscillatory or semi-conservative behaviour. Within this critical state, we can leverage results from the physics literature, which serve as analogues for neural fields, and implicit construct validity. Comparisons between our model predictions and electrophysiological findings from the literature - such as spectral power distribution across frequencies, wave propagation speed, epileptic seizure generation, and pattern formation over the cortical surface - demonstrate a close match. This study underscores the importance of utilizing symmetry preserving PDE formulations for further mechanistic insights into cortical activity.

Activity in layer 2/3 of the mouse primary visual cortex has been shown to depend both on visual input and the mouse's locomotion. Moreover, this activity is altered by a mismatch between the observed visual flow and the predicted visual flow from locomotion. Here, I present a simple computational model that explains previously reported recordings from layer 2/3 neurons in mice. In my model, layer 2/3 encodes the velocity difference between the estimate from visual flow and the prediction from locomotion using a neural population code. Moreover, I describe a hypothesized mechanism for how the brain may carry out computations of variables encoded in population codes. This mechanism may point to a general principle for computing any mathematical function in the brain.

The hippocampal formation is critical for episodic memory, with area Cornu Ammonis 3 (CA3) a necessary substrate for auto-associative pattern completion. Recent theoretical and experimental evidence suggests that the formation and retrieval of cell assemblies enable these functions. Yet, how cell assemblies are formed and retrieved in a full-scale spiking neural network (SNN) of CA3 that incorporates the observed diversity of neurons and connections within this circuit is not well understood. Here, we demonstrate that a data-driven SNN model quantitatively reflecting the neuron type-specific population sizes, intrinsic electrophysiology, connectivity statistics, synaptic signaling, and long-term plasticity of the mouse CA3 is capable of robust auto-association and pattern completion via cell assemblies. Our results show that a broad range of assembly sizes could successfully and systematically retrieve patterns from heavily incomplete or corrupted cues after a limited number of presentations. Furthermore, performance was robust with respect to partial overlap of assemblies through shared cells, substantially enhancing memory capacity. These novel findings provide computational evidence that the specific biological properties of the CA3 circuit produce an effective neural substrate for associative learning in the mammalian brain.

We demonstrate a model of chirp-velocity sensitivity in the inferior colliculus (IC) that retains the tuning to amplitude modulation (AM) that was established in earlier models. The mechanism of velocity sensitivity is sequence detection by octopus cells of the posteroventral cochlear nucleus, which have been proposed in physiological studies to respond preferentially to the order of arrival of cross-frequency inputs of different amplitudes. Model architecture is based on coincidence detection of a combination of excitatory and inhibitory inputs. Chirp-sensitivity of the IC output is largely controlled by the strength and timing of the chirp-sensitive octopus-cell inhibitory input. AM tuning is controlled by inhibition and excitation that are tuned to the same frequency. We present several example neurons that demonstrate the feasibility of the model in simulating realistic chirp-sensitivity and AM tuning for a wide range of characteristic frequencies. Additionally, we explore the systematic impact of varying parameters on model responses. The proposed model can be used to assess the contribution of IC chirp-velocity sensitivity to responses to complex sounds, such as speech.