Circuits that contain the Model Concept : Neuromodulation

(Neurotransmitters that act on a longer timescale than 200 milliseconds are called neuromodulators. They make cells easier or harder to excite in response to their ongoing glutamate and gaba inputs and frequently cause changes to potassium leak current conductance among other possibilities.)
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    Models   Description
1. A 1000 cell network model for Lateral Amygdala (Kim et al. 2013)
1000 Cell Lateral Amygdala model for investigation of plasticity and memory storage during Pavlovian Conditioning.
2. A two-layer biophysical olfactory bulb model of cholinergic neuromodulation (Li and Cleland 2013)
This is a two-layer biophysical olfactory bulb (OB) network model to study cholinergic neuromodulation. Simulations show that nicotinic receptor activation sharpens mitral cell receptive field, while muscarinic receptor activation enhances network synchrony and gamma oscillations. This general model suggests that the roles of nicotinic and muscarinic receptors in OB are both distinct and complementary to one another, together regulating the effects of ascending cholinergic inputs on olfactory bulb transformations.
3. Emergence of spatiotemporal sequences in spiking neuronal networks (Spreizer et al 2019)
"Spatio-temporal sequences of neuronal activity are observed in many brain regions in a variety of tasks and are thought to form the basis of meaningful behavior. However, mechanisms by which a neuronal network can generate spatio-temporal activity sequences have remained obscure. Existing models are biologically untenable because they either require manual embedding of a feedforward network within a random network or supervised learning to train the connectivity of a network to generate sequences. Here, we propose a biologically plausible, generative rule to create spatio-temporal activity sequences in a network of spiking neurons with distance-dependent connectivity. We show that the emergence of spatio- temporal activity sequences requires: (1) individual neurons preferentially project a small fraction of their axons in a specific direction, and (2) the preferential projection direction of neighboring neurons is similar. Thus, an anisotropic but correlated connectivity of neuron groups suffices to generate spatio-temporal activity sequences in an otherwise random neuronal network model."
4. Interaction of leak and IMI conductance on the STG over broad temperature range (Stadele et al 2015)
The ZIP file contains a Hodgkin-Huxley based circuit model and the simulation environment MadSim used to study the interaction of leak and IMI on the gastric mill network of the crab (Cancer borealis) as represented in (C. Städele, S. Heigele and W. Stein, 2015) MadSim, the simulation environment used for this study, is freeware and included in the package.
5. Multiscale model of excitotoxicity in PD (Muddapu and Chakravarthy 2020)
Parkinson's disease (PD) is a neurodegenerative disorder caused by loss of dopaminergic neurons in Substantia Nigra pars compacta (SNc). Although the exact cause of cell death is not clear, the hypothesis that metabolic deficiency is a key factor has been gaining attention in recent years. In the present study, we investigate this hypothesis using a multi-scale computational model of the subsystem of the basal ganglia comprising Subthalamic Nucleus (STN), Globus Pallidus externa (GPe) and SNc. The proposed model is a multiscale model in that interactions among the three nuclei are simulated using more abstract Izhikevich neuron models, while the molecular pathways involved in cell death of SNc neurons are simulated in terms of detailed chemical kinetics. Simulation results obtained from the proposed model showed that energy deficiencies occurring at cellular and network levels could precipitate the excitotoxic loss of SNc neurons in PD. At the subcellular level, the models show how calcium elevation leads to apoptosis of SNc neurons. The therapeutic effects of several neuroprotective interventions are also simulated in the model. From neuroprotective studies, it was clear that glutamate inhibition and apoptotic signal blocker therapies were able to halt the progression of SNc cell loss when compared to other therapeutic interventions, which only slows down the progression of SNc cell loss.
6. Muscle spindle feedback circuit (Moraud et al, 2016)
Here, we developed a computational model of the muscle spindle feedback circuits of the rat ankle that predicts the interactions between Epidural Stimulation and spinal circuit dynamics during gait.

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