Modulating excitability in the cortical network: impact on emergent activity and traveling waves

2014 ◽  
Vol 1 ◽  
pp. 563-565
Author(s):  
M.V. Sanchez-Vives ◽  
Maurizio Mattia
Keyword(s):  
Traveling Waves ◽  
Cortical Network

scholarly journals Tagged MEG measures binocular rivalry in a cortical network that predicts alternation rate

PLoS ONE ◽  
2019 ◽  
Vol 14 (7) ◽  
pp. e0218529 ◽  
Author(s):  
Elizabeth A. Bock ◽  
Jeremy D. Fesi ◽  
Sylvain Baillet ◽  
Janine D. Mendola
Keyword(s):  
Binocular Rivalry ◽  
Cortical Network ◽  
Alternation Rate

Double-Diffusive Convection in Traveling Waves in the Iodate−Sulfite System Explained

1996 ◽  
Vol 100 (40) ◽  
pp. 16209-16212 ◽  
Author(s):  
John A. Pojman ◽  
Andrea Komlósi ◽  
Istvan P. Nagy
Keyword(s):  
Traveling Waves ◽  
Double Diffusive Convection ◽  
Diffusive Convection ◽  
Double Diffusive

Existence of traveling waves in Fermi–Pasta–Ulam–type systems on a 2D–lattice

2021 ◽  
Vol 252 (4) ◽  
pp. 453-462
Author(s):  
Sergiy Mykolayovych Bak ◽  
Galyna Mykolayivna Kovtonyuk
Keyword(s):  
Traveling Waves ◽  
Type Systems

scholarly journals Altered network properties in C9ORF72 repeat expansion cortical neurons are due to synaptic dysfunction

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Emma M. Perkins ◽  
Karen Burr ◽  
Poulomi Banerjee ◽  
Arpan R. Mehta ◽  
Owen Dando ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Synaptic Vesicle ◽  
Cortical Neurons ◽  
Electrode Array ◽  
Repeat Expansion ◽  
Cortical Network ◽  
Synaptic Function ◽  
Network Activity ◽  
Cortical Function ◽  
Network Function

Abstract Background Physiological disturbances in cortical network excitability and plasticity are established and widespread in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) patients, including those harbouring the C9ORF72 repeat expansion (C9ORF72RE) mutation – the most common genetic impairment causal to ALS and FTD. Noting that perturbations in cortical function are evidenced pre-symptomatically, and that the cortex is associated with widespread pathology, cortical dysfunction is thought to be an early driver of neurodegenerative disease progression. However, our understanding of how altered network function manifests at the cellular and molecular level is not clear. Methods To address this we have generated cortical neurons from patient-derived iPSCs harbouring C9ORF72RE mutations, as well as from their isogenic expansion-corrected controls. We have established a model of network activity in these neurons using multi-electrode array electrophysiology. We have then mechanistically examined the physiological processes underpinning network dysfunction using a combination of patch-clamp electrophysiology, immunocytochemistry, pharmacology and transcriptomic profiling. Results We find that C9ORF72RE causes elevated network burst activity, associated with enhanced synaptic input, yet lower burst duration, attributable to impaired pre-synaptic vesicle dynamics. We also show that the C9ORF72RE is associated with impaired synaptic plasticity. Moreover, RNA-seq analysis revealed dysregulated molecular pathways impacting on synaptic function. All molecular, cellular and network deficits are rescued by CRISPR/Cas9 correction of C9ORF72RE. Our study provides a mechanistic view of the early dysregulated processes that underpin cortical network dysfunction in ALS-FTD. Conclusion These findings suggest synaptic pathophysiology is widespread in ALS-FTD and has an early and fundamental role in driving altered network function that is thought to contribute to neurodegenerative processes in these patients. The overall importance is the identification of previously unidentified defects in pre and postsynaptic compartments affecting synaptic plasticity, synaptic vesicle stores, and network propagation, which directly impact upon cortical function.

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