scholarly journals When two wrongs make a right: synchronized neuronal bursting from combined electrical and inhibitory coupling

2017 ◽  
Vol 375 (2096) ◽  
pp. 20160282 ◽  
Author(s):  
Reimbay Reimbayev ◽  
Kevin Daley ◽  
Igor Belykh
Keyword(s):  
Electrical Coupling ◽  
Coupled System ◽  
Underlying Mechanism ◽  
Mathematical Methods ◽  
Synaptic Inputs ◽  
Bursting Neurons ◽  
Robust Synchronization ◽  
Neuronal Mechanisms ◽  
Central Nervous Systems ◽  
Inhibitory Coupling

Synchronized cortical activities in the central nervous systems of mammals are crucial for sensory perception, coordination and locomotory function. The neuronal mechanisms that generate synchronous synaptic inputs in the neocortex are far from being fully understood. In this paper, we study the emergence of synchronization in networks of bursting neurons as a highly non-trivial, combined effect of electrical and inhibitory connections. We report a counterintuitive find that combined electrical and inhibitory coupling can synergistically induce robust synchronization in a range of parameters where electrical coupling alone promotes anti-phase spiking and inhibition induces anti-phase bursting. We reveal the underlying mechanism, which uses a balance between hidden properties of electrical and inhibitory coupling to act together to synchronize neuronal bursting. We show that this balance is controlled by the duty cycle of the self-coupled system which governs the synchronized bursting rhythm. This article is part of the themed issue ‘Mathematical methods in medicine: neuroscience, cardiology and pathology’.

Phase Selective Oscillations in Two Noise Driven Synaptically Coupled Spiking Neurons

2015 ◽  
Vol 25 (07) ◽  
pp. 1540005
Author(s):  
Ilya Prokin ◽  
Ivan Tyukin ◽  
Victor Kazantsev
Keyword(s):  
Numerical Simulations ◽  
Coupled System ◽  
External Noise ◽  
Noise Signal ◽  
Feedback Mechanism ◽  
Spike Timing ◽  
Spiking Neurons ◽  
Time Lags ◽  
Tuning Parameters ◽  
Synaptic Inputs

The work investigates the influence of spike-timing dependent plasticity (STDP) mechanisms on the dynamics of two synaptically coupled neurons driven by additive external noise. In this setting, the noise signal models synaptic inputs that the pair receives from other neurons in a larger network. We show that in the absence of STDP feedbacks the pair of neurons exhibit oscillations and intermittent synchronization. When the synapse connecting the neurons is supplied with a phase selective feedback mechanism simulating STDP, induced dynamics of spikes in the coupled system resembles a phase locked mode with time lags between spikes oscillating about a specific value. This value, as we show by extensive numerical simulations, can be set arbitrary within a broad interval by tuning parameters of the STDP feedback.

The Integration of the Patterned Output of Buccal Motoneurones During Feeding in Tritonia Hombergi

1979 ◽  
Vol 79 (1) ◽  
pp. 23-40
Author(s):  
A.G. M. BULLOCH ◽  
D. A. DORSETT
Keyword(s):  
Feeding Activity ◽  
Electrical Coupling ◽  
Cell Activity ◽  
Giant Cells ◽  
Posterior Border ◽  
Buccal Ganglion ◽  
Synaptic Inputs ◽  
Proprioceptive Input ◽  
Buccal Ganglia ◽  
Feeding Cycle

Three phases of activity may be recognized in the buccal mass of Tritonia hombergi during the feeding cycle. These have been termed Protraction, Retraction and Flattening. Each phase is driven by a group of motoneurones along the posterior border of the buccal ganglia. The patterned bursting observed in the motoneurone groups during feeding activity is phased by synaptic inputs which are common to two or more groups. Evidence is presented which indicates these inputs are derived from three unidentified multi-action interneurone sources within each buccal ganglion, and whose action primarily determines the patterned output of the motoneurones. Electrical coupling between between synergistic motoneurones and, in one case, post-inhibitory rebound, contribute to the synchronization of group activity. Proprioceptive input to the motoneurones was not identified, but may project to the interneurones. Some small neurones having synaptic inputs on the motoneurones appropriate to two of the interneurones were found, but require confirmation in this role. The cerebral giant cells synapse on representatives of three motoneurone groups, and also activate the buccal interneurones driving the feeding cycle. The patterned activity of the motoneurones can occur in the absence of cerebral cell activity.

scholarly journals Using a Model to Assess the Role of the Spatiotemporal Pattern of Inhibitory Input and Intrasegmental Electrical Coupling in the Intersegmental and Side-to-Side Coordination of Motor Neurons by the Leech Heartbeat Central Pattern Generator

2008 ◽  
Vol 100 (3) ◽  
pp. 1354-1371 ◽  
Author(s):  
Paul S. García ◽  
Terrence M. Wright ◽  
Ian R. Cunningham ◽  
Ronald L. Calabrese
Keyword(s):  
Motor Neuron ◽  
Central Pattern Generator ◽  
Motor Neurons ◽  
Electrical Coupling ◽  
Pattern Generator ◽  
Living System ◽  
Phase Relations ◽  
Spatiotemporal Pattern ◽  
Intrinsic Properties ◽  
Synaptic Inputs

Previously we presented a quantitative description of the spatiotemporal pattern of inhibitory synaptic input from the heartbeat central pattern generator (CPG) to segmental motor neurons that drive heartbeat in the medicinal leech and the resultant coordination of CPG interneurons and motor neurons. To begin elucidating the mechanisms of coordination, we explore intersegmental and side-to-side coordination in an ensemble model of all heart motor neurons and their known synaptic inputs and electrical coupling. Model motor neuron intrinsic properties were kept simple, enabling us to determine the extent to which input and electrical coupling acting together can account for observed coordination in the living system in the absence of a substantive contribution from the motor neurons themselves. The living system produces an asymmetric motor pattern: motor neurons on one side fire nearly in synchrony (synchronous), whereas on the other they fire in a rear-to-front progression (peristaltic). The model reproduces the general trends of intersegmental and side-to-side phase relations among motor neurons, but the match with the living system is not quantitatively accurate. Thus realistic (experimentally determined) inputs do not produce similarly realistic output in our model, suggesting that motor neuron intrinsic properties may contribute to their coordination. By varying parameters that determine electrical coupling, conduction delays, intraburst synaptic plasticity, and motor neuron excitability, we show that the most important determinant of intersegmental and side-to-side phase relations in the model was the spatiotemporal pattern of synaptic inputs, although phasing was influenced significantly by electrical coupling.

scholarly journals Market clearing model of distribution network-side integrated energy system

2020 ◽  
Vol 165 ◽  
pp. 01019
Author(s):  
Dongmei Yang ◽  
Yong Sun ◽  
Baoju Li ◽  
Xiaochen Zhang ◽  
Pengfei Li ◽  
...  
Keyword(s):  
Electrical Coupling ◽  
Coupled System ◽  
Energy System ◽  
Energy Price ◽  
Price Setting ◽  
Energy Prices ◽  
Market Clearing ◽  
Coupling System ◽  
Integrated Energy System ◽  
Node Energy

In an electric-gas integrated energy system that considers the coupling conditions between systems, there is energy transaction between the systems. So the node energy price setting method and market clearing strategy of the coupled system are worth studying. First of all, this paper establishes a market clearing model for electricity / gas subsystems and a method for solving node energy prices. Then, a market clearing model of the electrical coupling system is established based on this. Finally, an example to verify the effectiveness of the nodal energy price formulation method and the market clearing model is given.

Synchronization Dynamics of Two Heterogeneous Chaotic Rulkov Neurons with Electrical Synapses

2017 ◽  
Vol 27 (02) ◽  
pp. 1730009 ◽  
Author(s):  
Lifang Cheng ◽  
Hongjun Cao
Keyword(s):  
Phase Synchronization ◽  
Spiking Neurons ◽  
Flip Bifurcation ◽  
Quiescent State ◽  
Complete Synchronization ◽  
Electrical Synapses ◽  
Bursting Neurons ◽  
Inhibitory Coupling ◽  
Burst Synchronization ◽  
Firing Neuron

Two heterogeneous chaotic Rulkov neurons with electrical synapses are investigated in this paper. First, we study the ability of the second neuron to modify the dynamics of the first neuron. It is shown that when the parameters of the first neuron are located at the vicinity of the Neimark–Sacker bifurcation curves the first firing neuron can be controlled into the quiescent state when coupled with the second neuron. While the parameters of the first neuron are near the flip bifurcation curves the first firing neuron cannot be suppressed. Second, we discuss burst synchronization for two bursting neurons and two tonic spiking neurons. It is shown that two heterogeneous chaotic Rulkov neurons with tonic spiking firing cannot reach anti-phase synchronization under the inhibitory coupling, which is different from the property of nonchaotic Rulkov neurons. Finally, we show that for two bursting neurons if the coupling is strong enough then burst synchronization can be converted into spike synchronization. However, complete synchronization cannot be achieved for any strong coupling.

4969Enhanced gap junction coupling organised and terminated acute ventricular fibrillation in ex-vivo perfused hearts

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
B S Handa ◽  
X Li ◽  
C Roney ◽  
D Pitcher ◽  
R A Chowdhury ◽  
...  
Keyword(s):  
Ventricular Fibrillation ◽  
Ex Vivo ◽  
Electrical Coupling ◽  
Underlying Mechanism ◽  
Dominant Frequency ◽  
Diffuse Fibrosis ◽  
Dependent Manner ◽  
Sprague Dawley ◽  
Concentration Dependent Manner

Abstract Background The underlying mechanism of ventricular fibrillation (VF) remains unclear. There are both experimental and clinical data to support the existence of rotational drivers (RDs), though other opposing studies suggest that VF is the result of disorganized myocardial activation. Abnormal electrical coupling between cardiomyocytes through gap junctions (GJ) has been considered an important factor in the genesis and maintenance of VF and pre-treatment with GJ couplers, rotigaptide (RTG), has been shown to reduce VF inducibility. Purpose We hypothesized that the degree of GJ coupling determines the underlying mechanism of VF, and that changes in GJ coupling can shift or modify the predominant mechanism of fibrillation along the spectrum between disorganised activity and organised drivers. We proposed that increased organisation of VF is critical to its termination. Methods Thirty Sprague-Dawley rat hearts were explanted, perfused ex-vivo and acute VF was induced with burst pacing and 30μM pinacidil. Optical mapping of transmembrane potential was performed at baseline and the effects of GJ coupling on VF dynamics were studied in an acute VF model by perfusing with increasing concentrations of a GJ uncoupler; carbenoxolone (0–50μM, CBX, n=10) or a GJ coupling-enhancer; RTG (0–80nM, n=10). A chronic diffuse fibrosis model (n=10) was generated with 4 weeks of in-vivo angiotensin infusion (500nm/kg/min). Fibrillation dynamics were quantified using phase analysis, phase singularity (PS) tracking and our novel method of global fibrillation organisation quantification, frequency dominance index (FDI), which is a power ratio of highest amplitude dominant frequency in the frequency spectrum. Results RTG increased average rotations per RD (Baseline: 2.86±0.10 vs 80nM: 5.66±0.43, p<0.001) whilst CBX caused a reduction (Baseline: 3.77±0.39 vs 50μM: 0.26±0.26, p<0.001). Maximum rotations for a RD increased with RTG (5.4±0.45 vs 48.20±12.32, p<0.001) and decreased with CBX (8.0±1.3 vs 0.3±0.3, p<0.001). Proportion of time PSs were detected in VF increased with RTG (0.44±0.06 vs 0.93±0.02, p<0.001) and decreased with CBX (0.61±0.9 vs 0.03±0.02, p<0.001). RTG reduced meander of longest duration RD (20.6±1.68 vs 11.51±0.77 pixels, p<0.001) for PS >5 rotations. FDI increased with RTG (0.53±0.04 vs 0.78±0.3, p<0.001) and decreased with CBX (0.60±0.05 vs 0.17±0.03, p<0.001). In the diffuse fibrosis group, in comparison to baseline RTG 80nM increased FDI (0.35 vs 0.65, p<0.001) and terminated VF in 40% of hearts. Conclusion The degree of GJ coupling is a key determinant of the underlying mechanism of VF. RTG organised fibrillation and stabilised RDs in a concentration-dependent manner whilst CBX disorganised VF. Enhancing GJ coupling with RTG in diseased hearts with fibrosis can terminate VF and may be a potential therapeutic target in acute VF. Acknowledgement/Funding BHF Programme Grant PG/16/17/32069

Analysis of Structure–Acoustic Coupling Characteristics Between Adjacent Flexible Panels and Enclosed Cavity

2020 ◽  
Vol 143 (2) ◽  
Author(s):  
Jie Zhang ◽  
Jian Pang ◽  
Yuping Wan ◽  
Liang Yang ◽  
Wenyu Jia ◽  
...  
Keyword(s):  
Coupling Effect ◽  
Structural Characteristics ◽  
Coupled System ◽  
Coupling Mechanism ◽  
Coupling Coefficients ◽  
Mathematical Methods ◽  
Modal Expansion ◽  
Acoustic Coupling ◽  
Coupling Characteristics ◽  
Flexible Panels

Abstract This article studies the structure–acoustic coupling mechanism between two adjacent flexible panels and an enclosed cavity by analytical and mathematical methods based on modal expansion methods and impedance mobility techniques. The results show that the coupling relations among subsystem modes of the coupled system have selectivity characteristics. The coupling strength depends on the normalized mode–shape coupling coefficients. The coupling relationship between two flexible panels is established through the enclosed cavity. The structural–acoustic coupling effect mainly affects the low-order modes of the coupled system, especially the first-order modes of the panels and cavity. When one panel is weakly coupled with the cavity, the two flexible panels are decoupled. The vibration of the panel only depends on its structural characteristics and external excitation, and the panel radiates sound into the cavity. The vibration of another panel depends not only on its structural characteristics but also on its coupling effect with the cavity.

scholarly journals NMDAR-dependent somatic potentiation of synaptic inputs is correlated with β amyloid-mediated neuronal hyperactivity

2021 ◽  
Vol 10 (1) ◽  
Author(s):  
Yifei Bao ◽  
Xin Yang ◽  
Yi Fu ◽  
Zhengyan Li ◽  
Ru Gong ◽  
...  
Keyword(s):  
Patch Clamp ◽  
Hippocampal Neurons ◽  
Single Channel ◽  
Early Stage ◽  
Glutamate Uptake ◽  
Hippocampal Slices ◽  
Underlying Mechanism ◽  
Open Probability ◽  
Synaptic Inputs ◽  
Β Amyloid

Abstract Background β Amyloid (Aβ)-mediated neuronal hyperactivity, a key feature of the early stage of Alzheimer’s disease (AD), is recently proposed to be initiated by the suppression of glutamate reuptake. Nevertheless, the underlying mechanism by which the impaired glutamate reuptake causes neuronal hyperactivity remains unclear. Chronic suppression of the glutamate reuptake causes accumulation of ambient glutamate that could diffuse from synaptic sites at the dendrites to the soma to elevate the tonic activation of somatic N-methyl-D-aspartate receptors (NMDARs). However, less attention has been paid to the potential role of tonic activity change in extrasynaptic glutamate receptors (GluRs) located at the neuronal soma on generation of neuronal hyperactivity. Methods Whole-cell patch-clamp recordings were performed on CA1 pyramidal neurons in acute hippocampal slices exposed to TFB-threo-β-benzyloxyaspartic acid (TBOA) or human Aβ1–42 peptide oligomer. A series of dendritic patch-clamp recordings were made at different distances from the soma to identify the location of the changes in synaptic inputs. Moreover, single-channel recording in the cell-attached mode was performed to investigate the activity changes of single NMDARs at the soma. Results Blocking glutamate uptake with either TBOA or the human Aβ1–42 peptide oligomer elicited potentiation of synaptic inputs in CA1 hippocampal neurons. Strikingly, this potentiation  specifically occurred at the soma, depending on the activation of somatic GluN2B-containing NMDARs (GluN2B-NMDARs) and accompanied by a substantial and persistent increment in the open probability of somatic NMDARs. Blocking the activity of GluN2B-NMDARs at the soma completely reversed both the TBOA-induced or the Aβ1–42-induced somatic potentiation and neuronal hyperactivity. Conclusions The somatic potentiation of synaptic inputs may represent a novel amplification mechanism that elevates cell excitability and thus contributes to neuronal hyperactivity initiated by impaired glutamate reuptake in AD.

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