Ephaptic Coupling

2006 ◽  
pp. 699-699
Keyword(s):  
2021 ◽  
Author(s):  
Gabriel Moreno Cunha ◽  
Gilberto Corso ◽  
José Garcia Vivas Miranda ◽  
Gustavo Zampier Dos Santos Lima

Abstract In recent decades, there has been growing interest in the impact of electric fields generated in the brain. Transmembrane ionic currents originate electric fields in the extracellular space and are capable of affecting nearby neurons, a phenomenon called ephaptic neuronal communication. In the present work, the Quadratic Integrate-and-Trigger model (QIF-E) underwent an adjustment/improvement to include the ephaptic coupling behavior between neurons and their results are compared to the empirical results. In this way, the analysis tools are employed according to the neuronal activity regime: (i) for the subthreshold regime, the circular statistic is used to describe the phase differences between the input stimulus signal and the modeled membrane response; (ii) in the suprathreshold regime, the Population Vector and the Spike Field Coherence are employed to estimate phase preferences and the coupling intensity between the input stimulus and the Action Potentials. The results observed are i) in the subthreshold regime the values of the phase differences change with distinct frequencies of an input stimulus; ii) in the supra-threshold regime the preferential phase of Action Potentials changes for different frequencies. In addition, we explore other parameters of the model, such as noise and membrane characteristic-time, in order to understand different types of neurons and extracellular environment related to ephaptic communication. Such results are consistent with results observed in empirical experiments based on ephaptic coupling behavior. In addition, the QIF-E model allows further studies on the physiological importance of ephaptic coupling in the brain, and its simplicity can open a door to simulating ephaptic coupling in neuron networks and evaluating the impact of ephaptic communication in such scenarios.


2020 ◽  
Vol 118 (3) ◽  
pp. 494a
Author(s):  
Joyce Lin ◽  
Steven Poelzing ◽  
Sharon A. George ◽  
Amara Greer-Short ◽  
Matthew W. Kay

2013 ◽  
Vol 60 (2) ◽  
pp. 576-582 ◽  
Author(s):  
Joyce Lin ◽  
James P. Keener

Author(s):  
Anastassiou Costas ◽  
Perin Rodrigo ◽  
Markram Henry ◽  
Koch Christof

NeuroSci ◽  
2021 ◽  
Vol 2 (3) ◽  
pp. 291-304
Author(s):  
Johnjoe McFadden

The conscious electromagnetic information (cemi) field theory proposes that the seat of consciousness is the brain’s electromagnetic (EM) field that integrates information from trillions of firing neurons. What we call free will is its output. The cemi theory also proposes that the brain has two streams. Most actions are initiated by the first non-conscious stream that is composed of neurons that are insulated from EM field influences. These non-conscious involuntary actions are thereby invisible to our EM field-located thoughts. The theory also proposes that voluntary actions are driven by neurons that receive EM field inputs and are thereby visible to our EM field-located thoughts. I review the extensive evidence for EM field/ephaptic coupling between neurons and the increasing evidence that EM fields in the brain are a cause of behaviour. I conclude by arguing that though this EM field-driven will is not free, in the sense of being acausal, it nevertheless corresponds to the very real experience of our conscious mind being in control of our voluntary actions. Will is not an illusion. It is our experience of control by our EM field-located mind. It is an immaterial, yet physical, will.


2018 ◽  
Vol 114 (3) ◽  
pp. 623a ◽  
Author(s):  
Gregory S. Hoeker ◽  
Carissa C. James ◽  
Sarah H. Barrett ◽  
James W. Smyth ◽  
Steven Poelzing

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Rengasayee Veeraraghavan ◽  
Joyce T Lin ◽  
James P Keener ◽  
Steven Poelzing ◽  
Robert G Gourdie

Pore-forming (Nav1.5) and auxiliary (β1; SCN1b) subunits of cardiac sodium channels are enriched at the cardiomyocyte intercalated disk (ID). Mathematical models suggest that this may facilitate conduction via ephaptic mechanisms. We recently demonstrated Nav1.5 enrichment (gSTED superresolution microscopy) and close membrane apposition (<10 nm; electron microscopy) within the perinexus, a microdomain surrounding connexin43 (Cx43) gap junctions (GJ). These data identified the perinexus as a candidate structure for the cardiac ephapse. Further studies using gSTED and STORM superresolution microscopy revealed Nav1.5 and β1 enrichment within ID regions not containing dense clusters of Cx43 and N-Cadherin. Notably, both were identified within the perinexus: Overall, 22% of Nav1.5 & β1 were located within perinexal regions while only 2 and 5% respectively overlapped with Cx43 clusters. Importantly, acute interstitial edema (AIE) increased intermembrane distance at perinexal, but not at non-perinexal sites in adult guinea pig myocardium. Functionally, this correlated with decreased transverse conduction velocity (CV-T; 15.2±0.3 vs. 19.6±0.1cm/s) and increased anisotropic ratio (AR; 3.0±0.2 vs. 2.8±0.1) relative to control, in perfused guinea pig ventricles. Nav1.5 blockade (0.5 μM flecainide) by itself decreased CV (18%) without changing AR. However, Nav1.5 inhibition during AIE preferentially decreased CV-T (13.0±0.6cm/s), increased AR (3.3±0.2) and increased spontaneous arrhythmias (7/9 vs. 4/11) compared to AIE alone. Notably, only a computer model including ephaptic coupling and the ID localization of Nav1.5 could recapitulate these results. Next we investigated the role of β1 in ephaptic coupling: Electrical cell-substrate impedance spectroscopy of 1610 cells heterologously overexpressing β1 revealed 3-fold higher paracellular resistance relative to native 1610 cells. These data along with the known cell adhesion function of β1 in neural tissue suggest that β1-mediated adhesion may facilitate close membrane apposition within the perinexus. Taken together, our results identify β1-mediated adhesion as a novel determinant of anisotropic conduction and potential antiarrhythmic target.


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