scholarly journals Itinerant complexity in networks of intrinsically bursting neurons

2020 ◽  
Vol 30 (6) ◽  
pp. 061106
Author(s):  
Siva Venkadesh ◽  
Ernest Barreto ◽  
Giorgio A. Ascoli
Keyword(s):  
Bursting Neurons

Exact synchronization of noisy bursting neurons with coupling delays

2009 ◽  
Vol 40 (3) ◽  
pp. 1127-1135 ◽  
Author(s):  
Nikola Burić ◽  
Kristina Todorović ◽  
Nebojša Vasović
Keyword(s):  
Bursting Neurons

scholarly journals Possible mechanisms underlying intermittent synchronous activity in the networks of excitatory and inhibitory bursting neurons

2011 ◽  
Vol 12 (S1) ◽  
Author(s):  
Choongseok Park ◽  
Leonid L Rubchinsky
Keyword(s):  
Synchronous Activity ◽  
Bursting Neurons

Models of Respiratory Rhythm Generation in the Pre-Bötzinger Complex. I. Bursting Pacemaker Neurons

1999 ◽  
Vol 82 (1) ◽  
pp. 382-397 ◽  
Author(s):  
Robert J. Butera ◽  
John Rinzel ◽  
Jeffrey C. Smith
Keyword(s):  
Membrane Potential ◽  
Respiratory Rhythm ◽  
Rhythm Generation ◽  
Minimal Models ◽  
Dynamic Features ◽  
Bursting Neurons ◽  
Wide Range ◽  
Bötzinger Complex ◽  
Voltage Dependent ◽  
Respiratory Rhythm Generation

A network of oscillatory bursting neurons with excitatory coupling is hypothesized to define the primary kernel for respiratory rhythm generation in the pre-Bötzinger complex (pre-BötC) in mammals. Two minimal models of these neurons are proposed. In model 1, bursting arises via fast activation and slow inactivation of a persistent Na+ current I NaP-h. In model 2, bursting arises via a fast-activating persistent Na+ current INaP and slow activation of a K+ current IKS. In both models, action potentials are generated via fast Na+ and K+currents. The two models have few differences in parameters to facilitate a rigorous comparison of the two different burst-generating mechanisms. Both models are consistent with many of the dynamic features of electrophysiological recordings from pre-BötC oscillatory bursting neurons in vitro, including voltage-dependent activity modes (silence, bursting, and beating), a voltage-dependent burst frequency that can vary from 0.05 to >1 Hz, and a decaying spike frequency during bursting. These results are robust and persist across a wide range of parameter values for both models. However, the dynamics of model 1 are more consistent with experimental data in that the burst duration decreases as the baseline membrane potential is depolarized and the model has a relatively flat membrane potential trajectory during the interburst interval. We propose several experimental tests to demonstrate the validity of either model and to differentiate between the two mechanisms.

Computer simulations of stimulus dependent state switching in basic circuits of bursting neurons

1998 ◽  
Vol 58 (5) ◽  
pp. 6418-6430 ◽  
Author(s):  
Mikhail Rabinovich ◽  
Ramón Huerta ◽  
Maxim Bazhenov ◽  
Alexander K. Kozlov ◽  
Henry D. I. Abarbanel
Keyword(s):  
Computer Simulations ◽  
Bursting Neurons ◽  
State Switching ◽  
Dependent State

A FINITE AUTOMATA MODEL OF SPIKING-BURSTING NEURONS

1996 ◽  
Vol 06 (04) ◽  
pp. 705-714 ◽  
Author(s):  
R. HUERTA
Keyword(s):  
Computer Modelling ◽  
Finite Automata ◽  
Central Pattern Generators ◽  
Qualitative Behavior ◽  
Experimental Measurements ◽  
Qualitative Model ◽  
Open Chain ◽  
Pacemaker Neurons ◽  
Bursting Neurons ◽  
Pattern Generators

A simple qualitative model of spiking-bursting neurons is proposed. It is mainly built from the qualitative behavior observed in central pattern generators (CPG’s) and pacemaker neurons. It is a finite automata which is convenient for computer modelling even for large neural networks. The number of rules utilized in the finite automata are the minimum necessary to reproduce a great variety of phenomena. The validity of the model is determined using actual experimental measurements between two coupled neurons in CPG’s. We reproduce, in the framework of the model, the dynamic patterns observed in Tritonia’s escape swimming CPG. Finally, we study the dynamics of an open chain of 100 reciprocally coupled “symbolic neurons” and investigate the stable patterns reached with time.

Excitatory effects induced by carbachol on bursting neurons of the rat subiculum

1996 ◽  
Vol 219 (1) ◽  
pp. 1-4 ◽  
Author(s):  
Hiroto Kawasaki ◽  
Massimo Avoli
Keyword(s):  
Bursting Neurons

Phase synchronization and its transition in two coupled bursting neurons: theoretical and numerical analysis

2010 ◽  
Vol 19 (6) ◽  
pp. 060509 ◽  
Author(s):  
Wang Hai-Xia ◽  
Lu Qi-Shao ◽  
Shi Xia
Keyword(s):  
Numerical Analysis ◽  
Phase Synchronization ◽  
Bursting Neurons ◽  
Theoretical And Numerical Analysis

Ionic Mechanisms Underlying Burst Firing of Layer III Sensorimotor Cortical Neurons of the Cat: An In Vitro Slice Study

2001 ◽  
Vol 86 (2) ◽  
pp. 771-781 ◽  
Author(s):  
Yoshihiro Nishimura ◽  
Masaru Asahi ◽  
Koichi Saitoh ◽  
Hirofumi Kitagawa ◽  
Yuichi Kumazawa ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Burst Firing ◽  
Ammonium Bromide ◽  
Channel Blockers ◽  
Main Function ◽  
Channel Blockade ◽  
Initial Burst ◽  
Bursting Neurons ◽  
Ionic Mechanisms

We examined the ionic mechanisms underlying burst firing in layer III neurons from cat sensorimotor cortex by intracellular recording in a brain slice. Regular spiking was observed in 77.4% of 137 neurons in response to constant intracellular current pulses of 0.5- to 1-s duration. The rest of the neurons showed burst firing. An initial burst followed by regular-spike firing was seen in 71.0% of 31 bursting neurons. The rest of the bursting neurons ( n = 9) exhibited repetitive bursting. In the bursting neurons, spikes comprising the burst were triggered from the afterdepolarization (ADP) of the first spike of the burst. We examined the ionic mechanisms underlying the ADP by applying channel-blocking agents. The ADP was enhanced (rather than blocked) by Ca2+ channel blockade. This enhancement of the ADP by Ca2+channel blockade was apparent even after blockade of the afterhyperpolarization by apamin or intracellular Ca2+ chelation by EGTA. The firing rate of the regular-spiking cells was increased by apamin, intracellular EGTA or Ca2+ channel blockers. In 17.9% of the neurons examined ( n = 56), these agents switched the regular-spiking pattern into a bursting one. Burst firing could not be changed to regular spiking by these agents. Four neurons that responded with a single initial burst in control solution responded with repetitive bursting after application of these agents. We conclude that the main function of Ca2+ influx in layer III neurons is to activate Ca2+-dependent K+ conductance, which prevents or limits burst firing. At a time when spike amplitude was unchanged, the ADP was blocked and the burst firing changed to regular spiking by extracellularly applied tetrodotoxin (TTX) or intracellularly applied N-(2,6-dimethylphenylcarbamoylmethyl) triethyl ammonium bromide (QX314). We concluded that a TTX- and QX314-sensitive Na+ current underlies the ADP and therefore contributes to the burst firing of layer III neurons from the cat cortex.

Firing responses of bursting neurons with delayed feedback

2010 ◽  
Vol 31 (1) ◽  
pp. 61-71 ◽  
Author(s):  
Hui-Ying Wu ◽  
Peter A. Robinson ◽  
Jong Won Kim
Keyword(s):  
Delayed Feedback ◽  
Bursting Neurons
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