Models that contain the Implementer : Simoes-de-Souza, Fabio [fabio.souza at]

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    Models   Description
1.  Alcohol excites Cerebellar Golgi Cells by inhibiting the Na+/K+ ATPase (Botta et al.2010)
Patch-clamp in cerebellar slices and computer modeling show that ethanol excites Golgi cells by inhibiting the Na+/K+ ATPase. In particular, voltage-clamp recordings of Na+/K+ ATPase currents indicated that ethanol partially inhibits this pump and this effect could be mimicked by low concentrations of the Na+/K+ ATPase blocker ouabain. The partial inhibition of Na+/K+ ATPase in a computer model of the Golgi cell reproduced these experimental findings that established a novel mechanism of action of ethanol on neural excitability.
2.  Cerebellar cortex oscil. robustness from Golgi cell gap jncs (Simoes de Souza and De Schutter 2011)
" ... Previous one-dimensional network modeling of the cerebellar granular layer has been successfully linked with a range of cerebellar cortex oscillations observed in vivo. However, the recent discovery of gap junctions between Golgi cells (GoCs), which may cause oscillations by themselves, has raised the question of how gap-junction coupling affects GoC and granular-layer oscillations. To investigate this question, we developed a novel two-dimensional computational model of the GoC-granule cell (GC) circuit with and without gap junctions between GoCs. ..."
3.  Granule Cells of the Olfactory Bulb (Simoes_De_Souza et al. 2014)
Electrical responses of three classes of granule cells of the olfactory bulb to synaptic activation in different dendritic locations. The constructed models were based on morphological detailed compartmental reconstructions of three granule cell classes of the olfactory bulb with active dendrites described by Bhalla and Bower (J. Neurophysiol. 69: 1948-1965, 1993) and dendritic spine distributions described by Woolf et al. (J. Neurosci. 11: 1837-1854, 1991). The computational studies with the model neurons showed that different quantities of spines have to be activated in each dendritic region to induce an action potential, which always was originated in the active terminal dendrites, independently of the location of the stimuli and the morphology of the dendritic tree.
4.  Mirror Neuron (Antunes et al 2017)
Modeling Mirror Neurons Through Spike-Timing Dependent Plasticity. This script reproduces Figure 3B.
5.  Molecular layer interneurons in cerebellum encode valence in associative learning (Ma et al 2020)
We used two-photon microscopy to study the role of ensembles of cerebellar molecular layer interneurons (MLIs) in a go-no go task where mice obtain a sugar water reward. In order to begin understanding the circuit basis of our findings in changes in lick behavior with chemogenetics in the go-no go associative learning olfactory discrimination task we generated a simple computational model of MLI interaction with PCs.
6.  Stochastic model of the olfactory cilium transduction and adaptation (Antunes et al 2014)
" ... In this work, we have combined stochastic computational modeling and a systematic pharmacological study of different signaling pathways to investigate their impact during short-term adaptation (STA). ... These results suggest that G-coupled receptors (GPCRs) cycling is involved with the occurrence of STA. To gain insights on the dynamical aspects of this process, we developed a stochastic computational model. The model consists of the olfactory transduction currents mediated by the cyclic nucleotide gated (CNG) channels and calcium ion (Ca2+)-activated chloride (CAC) channels, and the dynamics of their respective ligands, cAMP and Ca2+, and it simulates the EOG (electroolfactogram) results obtained under different experimental conditions through changes in the amplitude and duration of cAMP and Ca2+ response, two second messengers implicated with STA occurrence. The model reproduced the experimental data for each pharmacological treatment and provided a mechanistic explanation for the action of GPCR cycling in the levels of second messengers modulating the levels of STA. All together, these experimental and theoretical results indicate the existence of a mechanism of regulation of STA by signaling pathways that control GPCR cycling and tune the levels of second messengers in OSNs, and not only by CNG channel desensitization as previously thought. "

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