Models | Description | |

1. | A full-scale cortical microcircuit spiking network model (Shimoura et al 2018) | |

Reimplementation in BRIAN 2 simulator of a full-scale cortical microcircuit containing two cell types (excitatory and inhibitory) distributed in four layers, and represents the cortical network below a surface of 1 mm² (Potjans & Diesmann, 2014). | ||

2. | CN bushy, stellate neurons (Rothman, Manis 2003) (Brian 2) | |

This model is an updated version of Romain Brette's adaptation of Rothman & Manis (2003). The model now uses Brian 2 instead of Brian 1 and can be configured to use n cells instead of a single cell. The included figure shows that Brian 2 is more efficient than Brian 1 once the number of cells exceeds 1,000. | ||

3. | Inhibitory microcircuits for top-down plasticity of sensory representations (Wilmes & Clopath 2019) | |

"Rewards influence plasticity of early sensory representations, but the underlying changes in circuitry are unclear. Recent experimental findings suggest that inhibitory circuits regulate learning. In addition, inhibitory neurons are highly modulated by diverse long-range inputs, including reward signals. We, therefore, hypothesise that inhibitory plasticity plays a major role in adjusting stimulus representations. We investigate how top-down modulation by rewards interacts with local plasticity to induce long-lasting changes in circuitry. Using a computational model of layer 2/3 primary visual cortex, we demonstrate how interneuron circuits can store information about rewarded stimuli to instruct long-term changes in excitatory connectivity in the absence of further reward. In our model, stimulus-tuned somatostatin-positive interneurons develop strong connections to parvalbumin-positive interneurons during reward such that they selectively disinhibit the pyramidal layer henceforth. This triggers excitatory plasticity, leading to increased stimulus representation. We make specific testable predictions and show that this two-stage model allows for translation invariance of the learned representation." | ||

4. | Mesoscopic dynamics from AdEx recurrent networks (Zerlaut et al JCNS 2018) | |

We present a mean-field model of networks of Adaptive Exponential (AdEx) integrate-and-fire neurons, with conductance-based synaptic interactions. We study a network of regular-spiking (RS) excitatory neurons and fast-spiking (FS) inhibitory neurons. We use a Master Equation formalism, together with a semi-analytic approach to the transfer function of AdEx neurons to describe the average dynamics of the coupled populations. We compare the predictions of this mean-field model to simulated networks of RS-FS cells, first at the level of the spontaneous activity of the network, which is well predicted by the analytical description. Second, we investigate the response of the network to time-varying external input, and show that the mean-field model predicts the response time course of the population. Finally, to model VSDi signals, we consider a one-dimensional ring model made of interconnected RS-FS mean-field units. | ||

5. | Model of the hippocampus over the sleep-wake cycle using Hodgkin-Huxley neurons (Aussel et al 2018) | |

" ...we propose a computational model of the hippocampal formation based on a realistic topology and synaptic connectivity, and we analyze the effect of different changes on the network, namely the variation of synaptic conductances, the variations of the CAN channel conductance and the variation of inputs. By using a detailed simulation of intracerebral recordings, we show that this is able to reproduce both the theta-nested gamma oscillations that are seen in awake brains and the sharp-wave ripple complexes measured during slow-wave sleep. The results of our simulations support the idea that the functional connectivity of the hippocampus, modulated by the sleep-wake variations in Acetylcholine concentration, is a key factor in controlling its rhythms." | ||

6. | Modeling dendritic spikes and plasticity (Bono and Clopath 2017) | |

Biophysical model and reduced neuron model with voltage-dependent plasticity. | ||

7. | Modelling the effects of short and random proto-neural elongations (de Wiljes et al 2017) | |

"To understand how neurons and nervous systems first evolved, we need an account of the origins of neural elongations: why did neural elongations (axons and dendrites) first originate, such that they could become the central component of both neurons and nervous systems? Two contrasting conceptual accounts provide different answers to this question. Braitenberg's vehicles provide the iconic illustration of the dominant input-output (IO) view. Here, the basic role of neural elongations is to connect sensors to effectors, both situated at different positions within the body. For this function, neural elongations are thought of as comparatively long and specific connections, which require an articulated body involving substantial developmental processes to build. Internal coordination (IC) models stress a different function for early nervous systems. Here, the coordination of activity across extended parts of a multicellular body is held central, in particular, for the contractions of (muscle) tissue. An IC perspective allows the hypothesis that the earliest proto-neural elongations could have been functional even when they were initially simple, short and random connections, as long as they enhanced the patterning of contractile activity across a multicellular surface. The present computational study provides a proof of concept that such short and random neural elongations can play this role. ..." | ||

8. | Neuromuscular network model of gut motility (Barth et al 2017) | |

Here we develop an integrated neuromechanical model of the ENS and assess neurostimulation strategies for enhancing gut motility. The model includes a network of enteric neurons, smooth muscle fibers, and interstitial cells of Cajal, which regulate propulsion of a virtual pellet in a model of gut motility. | ||

9. | Response to correlated synaptic input for HH/IF point neuron vs with dendrite (Górski et al 2018) | |

" ... Here, we study computational models of neurons to investigate the functional effects of dendritic spikes. In agreement with previous studies, we found that point neurons or neurons with passive dendrites increase their somatic firing rate in response to the correlation of synaptic bombardment for a wide range of input conditions, i.e. input firing rates, synaptic conductances, or refractory periods. However, neurons with active dendrites show the opposite behavior: for a wide range of conditions the firing rate decreases as a function of correlation. We found this property in three types of models of dendritic excitability: a Hodgkin-Huxley model of dendritic spikes, a model with integrate and fire dendrites, and a discrete-state dendritic model. We conclude that fast dendritic spikes confer much broader computational properties to neurons, sometimes opposite to that of point neurons." | ||

10. | Robust modulation of integrate-and-fire models (Van Pottelbergh et al 2018) | |

"By controlling the state of neuronal populations, neuromodulators ultimately affect behavior. A key neuromodulation mechanism is the alteration of neuronal excitability via the modulation of ion channel expression. This type of neuromodulation is normally studied with conductance-based models, but those models are computationally challenging for large-scale network simulations needed in population studies. This article studies the modulation properties of the multiquadratic integrate-and-fire model, a generalization of the classical quadratic integrate-and-fire model. The model is shown to combine the computational economy of integrate-and-fire modeling and the physiological interpretability of conductance-based modeling. It is therefore a good candidate for affordable computational studies of neuromodulation in large networks." |