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| Models | Description |
| Cortical network model of posttraumatic epileptogenesis (Bush et al 1999) | |
| This simulation from Bush, Prince, and Miller 1999 shows the epileptiform response (Fig. 6C) to a brief single stimulation in a 500 cell network of multicompartment models, some of which have active dendrites. The results which I obtained under Redhat Linux is shown in result.gif. Original 1997 code from Paul Bush modified slightly by Bill Lytton to make it work with current version of NEURON (5.7.139). Thanks to Paul Bush and Ken Miller for making the code available. | |
| 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. ..." | |
| Network model with neocortical architecture (Anderson et al. 2011 plus under review paper) | |
| Architecturally realistic neocortical model using seven classes of excitatory and inhibitory single compartment Hodgkin-Huxley cells. This is an addendum to ModelDB Accession # 98902, Studies of stimulus parameters for seizure disruption (Anderson et al. 2007). Wiring is adapted from the minicolumn hypothesis and incorporates visual and neocortical wiring data. Simulation demonstrates spontaneous bursting onset and cessation. This activity can be induced by random fluctuations in the surrounding background input (Manuscript in preparation). | |
| Parametric computation and persistent gamma in a cortical model (Chambers et al. 2012) | |
| Using the Traub et al (2005) model of the cortex we determined how 33 synaptic strength parameters control gamma oscillations. We used fractional factorial design to reduce the number of runs required to 4096. We found an expected multiplicative interaction between parameters. | |
| Prosthetic electrostimulation for information flow repair in a neocortical simulation (Kerr 2012) | |
| This model is an extension of a model (138379) 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. | |
| Studies of stimulus parameters for seizure disruption using NN simulations (Anderson et al. 2007) | |
| Architecturally realistic neocortical model using seven classes of excitatory and inhibitory single compartment Hodgkin-Huxley cells. Wiring is adapted to minicolumn hypothesis and incorporates visual and neocortical data. Simulation demonstrates spontaneous bursting onset and cessation, and activity can be altered with external electric field. | |
| Surround Suppression in V1 via Withdraw of Balanced Local Excitation in V1 (Shushruth 2012) | |
| The model is mean-field network models, which is set up as a so-called ring-model, i. e. it is a highly idealized model of an orientation hypercolumn in primary visual cortex. Long-range intra-areal and inter-areal feedback connections are modeled phenomenologically as an external input. In this model, there are recurrent interactions via short-range local connections between orientation columns, but not between hypercolumns. | |
| 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." | |
| 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. | |
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