Models that contain the Implementer : Neymotin, Sam [Samuel.Neymotin at nki.rfmh.org]

Re-display model names without descriptions
    Models   Description
1.  Boolean network-based analysis of the apoptosis network (Mai and Liu 2009)
"To understand the design principles of the molecular interaction network associated with the irreversibility of cell apoptosis and the stability of cell surviving, we constructed a Boolean network integrating both the intrinsic and extrinsic pro-apoptotic pathways with pro-survival signal transduction pathways. We performed statistical analyses of the dependences of cell fate on initial states and on input signals. The analyses reproduced the well-known pro- and anti-apoptotic effects of key external signals and network components. We found that the external GF signal by itself did not change the apoptotic ratio from randomly chosen initial states when there is no external TNF signal, but can significantly offset apoptosis induced by the TNF signal. ..."
2.  Ca+/HCN channel-dependent persistent activity in multiscale model of neocortex (Neymotin et al 2016)
"Neuronal persistent activity has been primarily assessed in terms of electrical mechanisms, without attention to the complex array of molecular events that also control cell excitability. We developed a multiscale neocortical model proceeding from the molecular to the network level to assess the contributions of calcium regulation of hyperpolarization-activated cyclic nucleotide-gated (HCN) channels in providing additional and complementary support of continuing activation in the network. ..."
3.  CA3 Network Model of Epileptic Activity (Sanjay et. al, 2015)
This computational study investigates how a CA3 neuronal network consisting of pyramidal cells, basket cells and OLM interneurons becomes epileptic when dendritic inhibition to pyramidal cells is impaired due to the dysfunction of OLM interneurons. After standardizing the baseline activity (theta-modulated gamma oscillations), systematic changes are made in the connectivities between the neurons, as a result of step-wise impairment of dendritic inhibition.
4.  Computer models of corticospinal neurons replicate in vitro dynamics (Neymotin et al. 2017)
"Corticospinal neurons (SPI), thick-tufted pyramidal neurons in motor cortex layer 5B that project caudally via the medullary pyramids, display distinct class-specific electrophysiological properties in vitro: strong sag with hyperpolarization, lack of adaptation, and a nearly linear frequency-current (FI) relationship. We used our electrophysiological data to produce a pair of large archives of SPI neuron computer models in two model classes: 1. Detailed models with full reconstruction; 2. Simplified models with 6 compartments. We used a PRAXIS and an evolutionary multiobjective optimization (EMO) in sequence to determine ion channel conductances. ..."
5.  Cortical model with reinforcement learning drives realistic virtual arm (Dura-Bernal et al 2015)
We developed a 3-layer sensorimotor cortical network of consisting of 704 spiking model-neurons, including excitatory, fast-spiking and low-threshold spiking interneurons. Neurons were interconnected with AMPA/NMDA, and GABAA synapses. We trained our model using spike-timing-dependent reinforcement learning to control a virtual musculoskeletal human arm, with realistic anatomical and biomechanical properties, to reach a target. Virtual arm position was used to simultaneously control a robot arm via a network interface.
6.  Electrostimulation to reduce synaptic scaling driven progression of Alzheimers (Rowan et al. 2014)
"... As cells die and synapses lose their drive, remaining cells suffer an initial decrease in activity. Neuronal homeostatic synaptic scaling then provides a feedback mechanism to restore activity. ... The scaling mechanism increases the firing rates of remaining cells in the network to compensate for decreases in network activity. However, this effect can itself become a pathology, ... Here, we present a mechanistic explanation of how directed brain stimulation might be expected to slow AD progression based on computational simulations in a 470-neuron biomimetic model of a neocortical column. ... "
7.  Emergence of physiological oscillation frequencies in neocortex simulations (Neymotin et al. 2011)
"Coordination of neocortical oscillations has been hypothesized to underlie the "binding" essential to cognitive function. However, the mechanisms that generate neocortical oscillations in physiological frequency bands remain unknown. We hypothesized that interlaminar relations in neocortex would provide multiple intermediate loops that would play particular roles in generating oscillations, adding different dynamics to the network. We simulated networks from sensory neocortex using 9 columns of event-driven rule-based neurons wired according to anatomical data and driven with random white-noise synaptic inputs. ..."
8.  Hopfield and Brody model (Hopfield, Brody 2000) (NEURON+python)
Demonstration of Hopfield-Brody snychronization using artificial cells in NEURON+python.
9.  Ih tunes oscillations in an In Silico CA3 model (Neymotin et al. 2013)
" ... We investigated oscillatory control using a multiscale computer model of hippocampal CA3, where each cell class (pyramidal, basket, and oriens-lacunosum moleculare cells), contained type-appropriate isoforms of Ih. Our model demonstrated that modulation of pyramidal and basket Ih allows tuning theta and gamma oscillation frequency and amplitude. Pyramidal Ih also controlled cross-frequency coupling (CFC) and allowed shifting gamma generation towards particular phases of the theta cycle, effected via Ih’s ability to set pyramidal excitability. ..."
10.  Ketamine disrupts theta modulation of gamma in a computer model of hippocampus (Neymotin et al 2011)
"Abnormalities in oscillations have been suggested to play a role in schizophrenia. We studied theta-modulated gamma oscillations in a computer model of hippocampal CA3 in vivo with and without simulated application of ketamine, an NMDA receptor antagonist and psychotomimetic. Networks of 1200 multi-compartment neurons (pyramidal, basket and oriens-lacunosum moleculare, OLM, cells) generated theta and gamma oscillations from intrinsic network dynamics: basket cells primarily generated gamma and amplified theta, while OLM cells strongly contributed to theta. ..."
11.  Measuring neuronal identification quality in ensemble recordings (isoitools) (Neymotin et al. 2011)
"... Here we describe information theoretic measures of action potential waveform isolation applicable to any dataset, that have an intuitive, universal interpretation, and that are not dependent on the methods or choice of parameters for single unit isolation, and that have been validated using a dataset."
12.  Motor cortex microcircuit simulation based on brain activity mapping (Chadderdon et al. 2014)
"... We developed a computational model based primarily on a unified set of brain activity mapping studies of mouse M1. The simulation consisted of 775 spiking neurons of 10 cell types with detailed population-to-population connectivity. Static analysis of connectivity with graph-theoretic tools revealed that the corticostriatal population showed strong centrality, suggesting that would provide a network hub. ... By demonstrating the effectiveness of combined static and dynamic analysis, our results show how static brain maps can be related to the results of brain activity mapping."
13.  Multitarget pharmacology for Dystonia in M1 (Neymotin et al 2016)
" ... We developed a multiscale model of primary motor cortex, ranging from molecular, up to cellular, and network levels, containing 1715 compartmental model neurons with multiple ion channels and intracellular molecular dynamics. We wired the model based on electrophysiological data obtained from mouse motor cortex circuit mapping experiments. We used the model to reproduce patterns of heightened activity seen in dystonia by applying independent random variations in parameters to identify pathological parameter sets. ..."
14.  NEURON interfaces to MySQL and the SPUD feature extraction algorithm (Neymotin et al. 2008)
See the readme.txt for information on setting up this interface to a MySQL server from the NEURON simulator. Note the SPUD feature extraction algorithm includes its own readme in the spud directory.
15.  Neuronal dendrite calcium wave model (Neymotin et al, 2015)
"... We developed a reaction-diffusion model of an apical dendrite with diffusible inositol triphosphate (IP3 ), diffusible Ca2+, IP3 receptors (IP3 Rs), endoplasmic reticulum (ER) Ca2+ leak, and ER pump (SERCA) on ER. ... At least two modes of Ca2+ wave spread have been suggested: a continuous mode based on presumed relative homogeneity of ER within the cell; and a pseudo-saltatory model where Ca2+ regeneration occurs at discrete points with diffusion between them. We compared the effects of three patterns of hypothesized IP3 R distribution: 1. continuous homogeneous ER, 2. hotspots with increased IP3R density (IP3 R hotspots), 3. areas of increased ER density (ER stacks). All three modes produced Ca2+ waves with velocities similar to those measured in vitro (~50 - 90µm /sec). ... The measures were sensitive to changes in density and spacing of IP3 R hotspots and stacks. ... An extended electrochemical model, including voltage gated calcium channels and AMPA synapses, demonstrated that membrane priming via AMPA stimulation enhances subsequent Ca2+ wave amplitude and duration. Our modeling suggests that pharmacological targeting of IP3 Rs and SERCA could allow modulation of Ca2+ wave propagation in diseases where Ca2+ dysregulation has been implicated. "
16.  Prosthetic electrostimulation for information flow repair in a neocortical simulation (Kerr 2012)
This model is an extension of a model (<a href="http://senselab.med.yale.edu/ModelDB/ShowModel.asp?model=138379">138379</a>) recently published in Frontiers in Computational Neuroscience. This model consists of 4700 event-driven, rule-based neurons, wired according to anatomical data, and driven by both white-noise synaptic inputs and a sensory signal recorded from a rat thalamus. Its purpose is to explore the effects of cortical damage, along with the repair of this damage via a neuroprosthesis.
17.  Reinforcement learning of targeted movement (Chadderdon et al. 2012)
"Sensorimotor control has traditionally been considered from a control theory perspective, without relation to neurobiology. In contrast, here we utilized a spiking-neuron model of motor cortex and trained it to perform a simple movement task, which consisted of rotating a single-joint “forearm” to a target. Learning was based on a reinforcement mechanism analogous to that of the dopamine system. This provided a global reward or punishment signal in response to decreasing or increasing distance from hand to target, respectively. Output was partially driven by Poisson motor babbling, creating stochastic movements that could then be shaped by learning. The virtual forearm consisted of a single segment rotated around an elbow joint, controlled by flexor and extensor muscles. ..."
18.  Sensorimotor cortex reinforcement learning of 2-joint virtual arm reaching (Neymotin et al. 2013)
"... We developed a model of sensory and motor neocortex consisting of 704 spiking model-neurons. Sensory and motor populations included excitatory cells and two types of interneurons. Neurons were interconnected with AMPA/NMDA, and GABAA synapses. We trained our model using spike-timing-dependent reinforcement learning to control a 2-joint virtual arm to reach to a fixed target. ... "
19.  Synaptic information transfer in computer models of neocortical columns (Neymotin et al. 2010)
"... We sought to measure how the activity of the network alters information flow from inputs to output patterns. Information handling by the network reflected the degree of internal connectivity. ... With greater connectivity strength, the recurrent network translated activity and information due to contribution of activity from intrinsic network dynamics. ... At still higher internal synaptic strength, the network corrupted the external information, producing a state where little external information came through. The association of increased information retrieved from the network with increased gamma power supports the notion of gamma oscillations playing a role in information processing."
20.  Synaptic scaling balances learning in a spiking model of neocortex (Rowan & Neymotin 2013)
Learning in the brain requires complementary mechanisms: potentiation and activity-dependent homeostatic scaling. We introduce synaptic scaling to a biologically-realistic spiking model of neocortex which can learn changes in oscillatory rhythms using STDP, and show that scaling is necessary to balance both positive and negative changes in input from potentiation and atrophy. We discuss some of the issues that arise when considering synaptic scaling in such a model, and show that scaling regulates activity whilst allowing learning to remain unaltered.
21.  The virtual slice setup (Lytton et al. 2008)
"In an effort to design a simulation environment that is more similar to that of neurophysiology, we introduce a virtual slice setup in the NEURON simulator. The virtual slice setup runs continuously and permits parameter changes, including changes to synaptic weights and time course and to intrinsic cell properties. The virtual slice setup permits shocks to be applied at chosen locations and activity to be sampled intra- or extracellularly from chosen locations. ..."

Re-display model names without descriptions