Mechanisms of Zero-Lag Synchronization in Cortical Motifs

Zero-lag synchronization between distant cortical areas has been observed in a diversity of experimental data sets and between many different regions of the brain. Several computational mechanisms have been proposed to account for such isochronous synchronization in the presence of long conduction delays: Of these, the phenomenon of "dynamical relaying" - a mechanism that relies on a specific network motif - has proven to be the most robust with respect to parameter mismatch and system noise. Surprisingly, despite a contrary belief in the community, the common driving motif is an unreliable means of establishing zero-lag synchrony. Although dynamical relaying has been validated in empirical and computational studies, the deeper dynamical mechanisms and comparison to dynamics on other motifs is lacking. By systematically comparing synchronization on a variety of small motifs, we establish that the presence of a single reciprocally connected pair - a "resonance pair" - plays a crucial role in disambiguating those motifs that foster zero-lag synchrony in the presence of conduction delays (such as dynamical relaying) from those that do not (such as the common driving triad). Remarkably, minor structural changes to the common driving motif that incorporate a reciprocal pair recover robust zero-lag synchrony. The findings are observed in computational models of spiking neurons, populations of spiking neurons and neural mass models, and arise whether the oscillatory systems are periodic, chaotic, noise-free or driven by stochastic inputs. The influence of the resonance pair is also robust to parameter mismatch and asymmetrical time delays amongst the elements of the motif. We call this manner of facilitating zero-lag synchrony resonance-induced synchronization, outline the conditions for its occurrence, and propose that it may be a general mechanism to promote zero-lag synchrony in the brain.Comment: 41 pages, 12 figures, and 11 supplementary figure

Beta-rhythm oscillations and synchronization transition in network models of Izhikevich neurons: effect of topology and synaptic type

Despite their significant functional roles, beta-band oscillations are least understood. Synchronization in neuronal networks have attracted much attention in recent years with the main focus on transition type. Whether one obtains explosive transition or a continuous transition is an important feature of the neuronal network which can depend on network structure as well as synaptic types. In this study we consider the effect of synaptic interaction (electrical and chemical) as well as structural connectivity on synchronization transition in network models of Izhikevich neurons which spike regularly with beta rhythms. We find a wide range of behavior including continuous transition, explosive transition, as well as lack of global order. The stronger electrical synapses are more conducive to synchronization and can even lead to explosive synchronization. The key network element which determines the order of transition is found to be the clustering coefficient and not the small world effect, or the existence of hubs in a network. These results are in contrast to previous results which use phase oscillator models such as the Kuramoto model. Furthermore, we show that the patterns of synchronization changes when one goes to the gamma band. We attribute such a change to the change in the refractory period of Izhikevich neurons which changes significantly with frequency.Comment: 7 figures, 1 tabl

Spike frequency adaptation affects the synchronization properties of networks of cortical oscillators

Oscillations in many regions of the cortex have common temporal characteristics with dominant frequencies centered around the 40 Hz (gamma) frequency range and the 5–10 Hz (theta) frequency range. Experimental results also reveal spatially synchronous oscillations, which are stimulus dependent (Gray&Singer, 1987;Gray, König, Engel, & Singer, 1989; Engel, König, Kreiter, Schillen, & Singer, 1992). This rhythmic activity suggests that the coherence of neural populations is a crucial feature of cortical dynamics (Gray, 1994). Using both simulations and a theoretical coupled oscillator approach, we demonstrate that the spike frequency adaptation seen in many pyramidal cells plays a subtle but important role in the dynamics of cortical networks. Without adaptation, excitatory connections among model pyramidal cells are desynchronizing. However, the slow processes associated with adaptation encourage stable synchronous behavior

Two distinct desynchronization processes caused by lesions in globally coupled neurons

To accomplish a task, the brain works like a synchronized neuronal network where all the involved neurons work together. When a lesion spreads in the brain, depending on its evolution, it can reach a significant portion of relevant area. As a consequence, a phase transition might occur: the neurons desynchronize and cannot perform a certain task anymore. Lesions are responsible for either disrupting the neuronal connections or, in some cases, for killing the neuron. In this work, we will use a simplified model of neuronal network to show that these two types of lesions cause different types of desynchronization.Comment: 5 pages, 3 figure