scholarly journals Emergence of chimera states in a neuronal model of delayed oscillators

2021 ◽  
Vol 3 (3) ◽  
Author(s):  
Alessandra Lucchetti ◽  
Mogens H. Jensen ◽  
Mathias L. Heltberg
2020 ◽  
Vol 30 (13) ◽  
pp. 2050256
Author(s):  
Henry M. Mitchell ◽  
Peter Sheridan Dodds ◽  
J. Matthew Mahoney ◽  
Christopher M. Danforth

Chimera states — the coexistence of synchrony and asynchrony in a nonlocally-coupled network of identical oscillators — are often used as a model framework for epileptic seizures. Here, we explore the dynamics of chimera states in a network of modified Hindmarsh–Rose neurons, configured to reflect the graph of the mesoscale mouse connectome. Our model produces superficially epileptiform activity converging on persistent chimera states in a large region of a two-parameter space governing connections (a) between subcortices within a cortex and (b) between cortices. Our findings contribute to a growing body of literature suggesting mathematical models can qualitatively reproduce epileptic seizure dynamics.


2016 ◽  
Author(s):  
Daniele Quintella Mendes ◽  
Luís Alfredo V. Carvalho ◽  
Roseli S. Wedemann
Keyword(s):  

Symmetry ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 341
Author(s):  
Shaobo He ◽  
Hayder Natiq ◽  
Santo Banerjee ◽  
Kehui Sun

By applying the Adams-Bashforth-Moulton method (ABM), this paper explores the complexity and synchronization of a fractional-order laser dynamical model. The dynamics under the variance of derivative order q and parameters of the system have examined using the multiscale complexity algorithm and the bifurcation diagram. Numerical simulation outcomes demonstrate that the system generates chaos with the decreasing of q. Moreover, this paper designs the coupled fractional-order network of laser systems and subsequently obtains its numerical solution using ABM. These solutions have demonstrated chimera states of the proposed fractional-order laser network.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Chialin Cheng ◽  
Surya A. Reis ◽  
Emily T. Adams ◽  
Daniel M. Fass ◽  
Steven P. Angus ◽  
...  

AbstractMutations in MAPT (microtubule-associated protein tau) cause frontotemporal dementia (FTD). MAPT mutations are associated with abnormal tau phosphorylation levels and accumulation of misfolded tau protein that can propagate between neurons ultimately leading to cell death (tauopathy). Recently, a p.A152T tau variant was identified as a risk factor for FTD, Alzheimer's disease, and synucleinopathies. Here we used induced pluripotent stem cells (iPSC) from a patient carrying this p.A152T variant to create a robust, functional cellular assay system for probing pathophysiological tau accumulation and phosphorylation. Using stably transduced iPSC-derived neural progenitor cells engineered to enable inducible expression of the pro-neural transcription factor Neurogenin 2 (Ngn2), we generated disease-relevant, cortical-like glutamatergic neurons in a scalable, high-throughput screening compatible format. Utilizing automated confocal microscopy, and an advanced image-processing pipeline optimized for analysis of morphologically complex human neuronal cultures, we report quantitative, subcellular localization-specific effects of multiple kinase inhibitors on tau, including ones under clinical investigation not previously reported to affect tau phosphorylation. These results demonstrate the potential for using patient iPSC-derived ex vivo models of tauopathy as genetically accurate, disease-relevant systems to probe tau biochemistry and support the discovery of novel therapeutics for tauopathies.


2021 ◽  
Vol 31 (1) ◽  
pp. 013135
Author(s):  
Dawid Dudkowski ◽  
Krzysztof Czołczyński ◽  
Tomasz Kapitaniak

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