Modeling of Synchronous Behaviors of Excitatory and Inhibitory Neurons in Complex Neuronal Networks

Author(s):  
Zhiheng Liu ◽  
Xia Shi
2000 ◽  
Vol 83 (2) ◽  
pp. 808-827 ◽  
Author(s):  
P. E. Latham ◽  
B. J. Richmond ◽  
P. G. Nelson ◽  
S. Nirenberg

Many networks in the mammalian nervous system remain active in the absence of stimuli. This activity falls into two main patterns: steady firing at low rates and rhythmic bursting. How are these firing patterns generated? Specifically, how do dynamic interactions between excitatory and inhibitory neurons produce these firing patterns, and how do networks switch from one firing pattern to the other? We investigated these questions theoretically by examining the intrinsic dynamics of large networks of neurons. Using both a semianalytic model based on mean firing rate dynamics and simulations with large neuronal networks, we found that the dynamics, and thus the firing patterns, are controlled largely by one parameter, the fraction of endogenously active cells. When no endogenously active cells are present, networks are either silent or fire at a high rate; as the number of endogenously active cells increases, there is a transition to bursting; and, with a further increase, there is a second transition to steady firing at a low rate. A secondary role is played by network connectivity, which determines whether activity occurs at a constant mean firing rate or oscillates around that mean. These conclusions require only conventional assumptions: excitatory input to a neuron increases its firing rate, inhibitory input decreases it, and neurons exhibit spike-frequency adaptation. These conclusions also lead to two experimentally testable predictions: 1) isolated networks that fire at low rates must contain endogenously active cells and 2) a reduction in the fraction of endogenously active cells in such networks must lead to bursting.


1997 ◽  
Vol 77 (6) ◽  
pp. 3218-3225 ◽  
Author(s):  
Thomas H. Müller ◽  
D. Swandulla ◽  
H. U. Zeilhofer

Müller, Thomas H., D. Swandulla, and H. U. Zeilhofer. Synaptic connectivity in cultured hypothalamic neuronal networks. J. Neurophysiol. 77: 3218–3225, 1997. We have developed a novel approach to analyze the synaptic connectivity of spontaneously active networks of hypothalamic neurons in culture. Synaptic connections were identified by recording simultaneously from pairs of neurons using the whole cell configuration of the patch-clamp technique and testing for evoked postsynaptic current responses to electrical stimulation of one of the neurons. Excitatory and inhibitory responses were distinguished on the basis of their voltage and time dependence. The distribution of latencies between presynaptic stimulation and postsynaptic response showed multiple peaks at regular intervals, suggesting that responses via both monosynaptic and polysynaptic paths were recorded. The probability that an excitatory event is transmitted to another excitatory neuron and results in an above-threshold stimulation was found to be only one in three to four. This low value indicates that in addition to evoked synaptic responses other sources of excitatory drive must contribute to the spontaneous activity observed in these networks. The various types of synaptic connections (excitatory and inhibitory, monosynaptic, and polysynaptic) were counted, and the observations analyzed using a probabilistic model of the network structure. This analysis provides estimates for the ratio of inhibitory to excitatory neurons in the network (1:1.5) and for the ratio of postsynaptic cells receiving input from a single GABAergic or glutamatergic neuron (3:1). The total number of inhibitory synaptic connections was twice that of excitatory connections. Cell pairs mutually connected by an excitatory and an inhibitory synapse occurred significantly more often than predicted by a random process. These results suggests that the formation of neuronal networks in vitro is controlled by cellular mechanisms that favor inhibitory connections in general and specifically enhance the formation of reciprocal connections between pairs of excitatory and inhibitory neurons. These mechanisms may contribute to network formation and function in vivo.


2005 ◽  
Vol 17 (3) ◽  
pp. 557-608 ◽  
Author(s):  
Christoph Börgers ◽  
Nancy Kopell

Synchronous rhythmic spiking in neuronal networks can be brought about by the interaction between E-cells and Icells (excitatory and inhibitory cells). The I-cells gate and synchronize the E-cells, and the E-cells drive and synchronize the I-cells. We refer to rhythms generated in this way as PING (pyramidal-interneuronal gamma) rhythms. The PING mechanism requires that the drive II to the I-cells be sufficiently low; the rhythm is lost when II gets too large. This can happen in at least two ways. In the first mechanism, the I-cells spike in synchrony, but get ahead of the E-cells, spiking without being prompted by the E-cells. We call this phase walkthrough of the I-cells. In the second mechanism, the I-cells fail to synchronize, and their activity leads to complete suppression of the E-cells. Noisy spiking in the E-cells, generated by noisy external drive, adds excitatory drive to the I-cells and may lead to phase walkthrough. Noisy spiking in the I-cells adds inhibition to the E-cells and may lead to suppression of the E-cells. An analysis of the conditions under which noise leads to phase walkthrough of the I-cells or suppression of the E-cells shows that PING rhythms at frequencies far below the gamma range are robust to noise only if network parameter values are tuned very carefully. Together with an argument explaining why the PING mechanism does not work far above the gamma range in the presence of heterogeneity, this justifies the “G” in “PING.”


Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Shuang Zhang ◽  
Yang Wu ◽  
Ningren Cui ◽  
Chun Jiang

The critical neuronal networks for breathing control known to be located in the brainstem are still not fully understood. γ-Aminobutyric acid (GABA) is a neurotransmitter that not only plays an important role in the networks, but also allows investigational interventions to the networks. To gain a fast, local and reversible access to brainstem GABAergic neurons, we developed a strain of transgenic mice that expressed channelrhodopsin in a tandem with eYFP in GABAergic neurons directed by the glutamic acid decarboxylase 2 promotor, the Gad2-ChR mouse. We firstly studied eYFP fluorescence in brainstem tissue sections. Several groups of previously known GABAergic neurons were positively labelled. Breathing response to optostimulation and CO 2 challenge were then studied in the anesthetized mice in vivo . When the optostimulation was applied to the ventral surface of the brainstem, especially the medulla, phrenic nerve activity was remarkably inhibited. Surprisingly, we found that optostimulation to the dorsal surface of the brainstem induced significant augmentation of both breathing activity and CO 2 chemosensitivity in the Gad2-ChR mice. Both breathing frequency and integrated phrenic amplitude were augmented. The effect was reversible and fast reaching peaking activation within 1 min. With respect to ventilation responses, optostimulation was nearly as potent as the response to 6% CO 2 . In the presence of 6% CO 2 , optostimulation was still capable of enhancing breathing activity. The breathing stimulation effect of optical GABA activation was located to the medulla. These observations suggest that respiratory neuronal networks involve a disinhibitory projection from dorsal GABAergic neurons in the medulla to a group of unidentified inhibitory neurons that are actively inhibit central breathing activity.


2017 ◽  
Author(s):  
Duane Q. Nykamp ◽  
Daniel Friedman ◽  
Sammy Shaker ◽  
Maxwell Shinn ◽  
Michael Vella ◽  
...  

The emergent dynamics in networks of recurrently coupled spiking neurons depends on the interplay between single-cell dynamics and network topology. Most theoretical studies on network dynamics have assumed simple topologies, such as connections which are made randomly and independently with a fixed probability (Erdös-Rényi network) (ER), or all-to-all connected networks. However, recent findings from slice experiments suggest that the actual patterns of connectivity between cortical neurons are more structured than in the ER random network. Here we explore how introducing additional higher-order statistical structure into the connectivity can affect the dynamics in neuronal networks. Specifically, we consider networks in which the number of pre-synaptic and post-synaptic contacts for each neuron, the degrees, are drawn from a joint degree distribution. We derive mean-field equations for a single population of homogeneous neurons and for a network of excitatory and inhibitory neurons, where the neurons can have arbitrary degree distributions. Through analysis of the mean-field equations and simulation of networks of integrate-and-fire neurons, we show that such networks have potentially much richer dynamics than an equivalent ER network. Finally, we relate the degree distributions to so-called cortical motifs.


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