Circuits that contain the Model Type : Axon

Re-display model names without descriptions

	Models	Description
1.	Biologically Constrained Basal Ganglia model (BCBG model) (Lienard, Girard 2014)
		We studied the physiology and function of the basal ganglia through the design of mean-field models of the whole basal ganglia. The parameterizations are optimized with multi-objective evolutionary algorithm to respect best a collection of numerous anatomical data and electrophysiological data. The main outcomes of our study are: • The strength of the GPe to GPi/SNr connection does not support opposed activities in the GPe and GPi/SNr. • STN and MSN target more the GPe than the GPi/SNr. • Selection arises from the structure of the basal ganglia, without properly segregated direct and indirect pathways and without specific inputs from pyramidal tract neurons of the cortex. Selection is enhanced when the projection from GPe to GPi/SNr has a diffuse pattern.
2.	CA1 pyramidal cell: reconstructed axonal arbor and failures at weak gap junctions (Vladimirov 2011)
		Model of pyramidal CA1 cells connected by gap junctions in their axons. Cell geometry is based on anatomical reconstruction of rat CA1 cell (NeuroMorpho.Org ID: NMO_00927) with long axonal arbor. Model init_2cells.hoc shows failures of second spike propagation in a spike doublet, depending on conductance of an axonal gap junction. Model init_ring.hoc shows that spike failure result in reentrant oscillations of a spike in a loop of axons connected by gap junctions, where one gap junction is weak. The paper shows that in random networks of axons connected by gap junctions, oscillations are driven by single pacemaker loop of axons. The shortest loop, around which a spike can travel, is the most likely pacemaker. This principle allows us to predict the frequency of oscillations from network connectivity and visa versa. We propose that this type of oscillations corresponds to so-called fast ripples in epileptic hippocampus.
3.	Cortical Basal Ganglia Network Model during Closed-loop DBS (Fleming et al 2020)
		We developed a computational model of the cortical basal ganglia network to investigate closed-loop control of deep brain stimulation (DBS) for Parkinson’s disease (PD). The cortical basal ganglia network model incorporates the (i) the extracellular DBS electric field, (ii) antidromic and orthodromic activation of STN afferent fibers, (iii) the LFP detected at non-stimulating contacts on the DBS electrode and (iv) temporal variation of network beta-band activity within the thalamo-cortico-basal ganglia loop. The model facilitates investigation of clinically-viable closed-loop DBS control approaches, modulating either DBS amplitude or frequency, using an LFP derived measure of network beta-activity.
4.	Human tactile FA1 neurons (Hay and Pruszynski 2020)
		"... we show that synaptic integration across the complex signals from the first-order neuronal population could underlie human ability to accurately (< 3°) and rapidly process the orientation of edges moving across the fingertip. We first derive spiking models of human first-order tactile neurons that fit and predict responses to moving edges with high accuracy. We then use the model neurons in simulating the peripheral neuronal population that innervates a fingertip. We train classifiers performing synaptic integration across the neuronal population activity, and show that synaptic integration across first-order neurons can process edge orientations with high acuity and speed. ... our models suggest that integration of fast-decaying (AMPA-like) synaptic inputs within short timescales is critical for discriminating fine orientations, whereas integration of slow-decaying (NMDA-like) synaptic inputs supports discrimination of coarser orientations and maintains robustness over longer timescales"
5.	Mechanisms of very fast oscillations in axon networks coupled by gap junctions (Munro, Borgers 2010)
		Axons connected by gap junctions can produce very fast oscillations (VFOs, > 80 Hz) when stimulated randomly at a low rate. The models here explore the mechanisms of VFOs that can be seen in an axonal plexus, (Munro & Borgers, 2009): a large network model of an axonal plexus, small network models of axons connected by gap junctions, and an implementation of the model underlying figure 12 in Traub et al. (1999) . The large network model consists of 3,072 5-compartment axons connected in a random network. The 5-compartment axons are the 5 axonal compartments from the CA3 pyramidal cell model in Traub et al. (1994) with a fixed somatic voltage. The random network has the same parameters as the random network in Traub et al. (1999), and axons are stimulated randomly via a Poisson process with a rate of 2/s/axon. The small network models simulate waves propagating through small networks of axons connected by gap junctions to study how local connectivity affects the refractory period.
6.	Neocort. pyramidal cells subthreshold somatic voltage controls spike propagation (Munro Kopell 2012)
		There is suggestive evidence that pyramidal cell axons in neocortex may be coupled by gap junctions into an ``axonal plexus" capable of generating Very Fast Oscillations (VFOs) with frequencies exceeding 80 Hz. It is not obvious, however, how a pyramidal cell in such a network could control its output when action potentials are free to propagate from the axons of other pyramidal cells into its own axon. We address this problem by means of simulations based on 3D reconstructions of pyramidal cells from rat somatosensory cortex. We show that somatic depolarization enables propagation via gap junctions into the initial segment and main axon, while somatic hyperpolarization disables it. We show further that somatic voltage cannot effectively control action potential propagation through gap junctions on minor collaterals; action potentials may therefore propagate freely from such collaterals regardless of somatic voltage. In previous work, VFOs are all but abolished during the hyperpolarization phase of slow-oscillations induced by anesthesia in vivo. This finding constrains the density of gap junctions on collaterals in our model and suggests that axonal sprouting due to cortical lesions may result in abnormally high gap junction density on collaterals, leading in turn to excessive VFO activity and hence to epilepsy via kindling.
7.	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.
8.	Principles of Computational Modelling in Neuroscience (Book) (Sterratt et al. 2011)
		"... This book provides a step-by-step account of how to model the neuron and neural circuitry to understand the nervous system at all levels, from ion channels to networks. Starting with a simple model of the neuron as an electrical circuit, gradually more details are added to include the effects of neuronal morphology, synapses, ion channels and intracellular signaling. The principle of abstraction is explained through chapters on simplifying models, and how simplified models can be used in networks. This theme is continued in a final chapter on modeling the development of the nervous system. Requiring an elementary background in neuroscience and some high school mathematics, this textbook is an ideal basis for a course on computational neuroscience."
9.	Response properties of neocort. neurons to temporally modulated noisy inputs (Koendgen et al. 2008)
		Neocortical neurons are classified by current–frequency relationship. This is a static description and it may be inadequate to interpret neuronal responses to time-varying stimuli. Theoretical studies (Brunel et al., 2001; Fourcaud-Trocmé et al. 2003; Fourcaud-Trocmé and Brunel 2005; Naundorf et al. 2005) suggested that single-cell dynamical response properties are necessary to interpret ensemble responses to fast input transients. Further, it was shown that input-noise linearizes and boosts the response bandwidth, and that the interplay between the barrage of noisy synaptic currents and the spike-initiation mechanisms determine the dynamical properties of the firing rate. In order to allow a reader to explore such simulations, we prepared a simple NEURON implementation of the experiments performed in Köndgen et al., 2008 (see also Fourcaud-Trocmé al. 2003; Fourcaud-Trocmé and Brunel 2005). In addition, we provide sample MATLAB routines for exploring the sandwich model proposed in Köndgen et al., 2008, employing a simple frequdency-domain filtering. The simulations and the MATLAB routines are based on the linear response properties of layer 5 pyramidal cells estimated by injecting a superposition of a small-amplitude sinusoidal wave and a background noise, as in Köndgen et al., 2008.
10.	State dependent drug binding to sodium channels in the dentate gyrus (Thomas & Petrou 2013)
		A Markov model of sodium channels was developed that includes drug binding to fast inactivated states. This was incorporated into a model of the dentate gyrus to investigate the effects of anti-epileptic drugs on neuron and network properties.
11.	Stoney vs Histed: Quantifying spatial effects of intracortical microstims (Kumaravelu et al 2022)
		"...We implemented a biophysically-based computational model of a cortical column comprising neurons with realistic morphology and representative synapses. We quantified the spatial effects of single pulses and short trains of ICMS, including the volume of activated neurons and the density of activated neurons as a function of stimulation intensity..."
12.	Striatal NN model of MSNs and FSIs investigated effects of dopamine depletion (Damodaran et al 2015)
		This study investigates the mechanisms that are affected in the striatal network after dopamine depletion and identifies potential therapeutic targets to restore normal activity.
13.	Synaptic gating at axonal branches, and sharp-wave ripples with replay (Vladimirov et al. 2013)
		The computational model of in vivo sharp-wave ripples with place cell replay. Excitatory post-synaptic potentials at dendrites gate antidromic spikes arriving from the axonal collateral, and thus determine when the soma and the main axon fire. The model allows synchronous replay of pyramidal cells during sharp-wave ripple event, and the replay is possible in both forward and reverse directions.
14.	Thalamic network model of deep brain stimulation in essential tremor (Birdno et al. 2012)
		"... Thus the decreased effectiveness of temporally irregular DBS trains is due to long pauses in the stimulus trains, not the degree of temporal irregularity alone. We also conducted computer simulations of neuronal responses to the experimental stimulus trains using a biophysical model of the thalamic network. Trains that suppressed tremor in volunteers also suppressed fluctuations in thalamic transmembrane potential at the frequency associated with cerebellar burst-driver inputs. Clinical and computational findings indicate that DBS suppresses tremor by masking burst-driver inputs to the thalamus and that pauses in stimulation prevent such masking. Although stimulation of other anatomic targets may provide tremor suppression, we propose that the most relevant neuronal targets for effective tremor suppression are the afferent cerebellar fibers that terminate in the thalamus."
15.	Vertical System (VS) tangential cells network model (Trousdale et al. 2014)
		Network model of the VS tangential cell system, with 10 cells per hemisphere. Each cell is a two compartment model with one compartment for dendrites and one for the axon. The cells are coupled through axonal gap junctions. The code allows to simulate responses of the VS network to a variety of visual stimuli to investigate coding as a function of gap junction strength.

Re-display model names without descriptions