The study of synchronization and bursting transition is very important and valuable in cognitive activities and action control of brain as well as enhancement for the reliability of the cortex synapses. However, we wo...The study of synchronization and bursting transition is very important and valuable in cognitive activities and action control of brain as well as enhancement for the reliability of the cortex synapses. However, we wonder how the synaptic strength and synaptic delay, especially the asymmetrical time-delays between different neurons can collectively influence their synchronous firing behaviors. In this paper, based on the Hindmarsh-Rose neuronal systems with asymmetrical time-delays, we investigate the collective effects of various delays and coupling strengths on the synchronization and bursting transition. It is shown that the interplay between delay and coupling strength can not only enhance or destroy the synchronizations but also can induce the regular transitions of bursting firing patterns. Specifically, as the coupling strength or time-delay increasing, the firing patterns of the time-delayed coupling neuronal systems consistently present a regular transition, that is, the periods of spikes during the bursting firings increase firstly and then decrease slowly. In particular, in contrast to the case of symmetrical time-delays,asymmetrical time-delays can lead to the paroxysmal synchronizations of coupling neuronal systems, as well as the concentration level of synchronization for the non-identically coupled system is superior to the one of identical coupling. These results more comprehensively reveal the rich nonlinear dynamical behaviors of neuronal systems and may be helpful for us to have a better understanding of the neural coding.展开更多
An autapse is an unusual synapse that occurs between the axon and the soma of the same neuron. Mathematically, it can be described as a self-delayed feedback loop that is defined by a specific time-delay and the so-ca...An autapse is an unusual synapse that occurs between the axon and the soma of the same neuron. Mathematically, it can be described as a self-delayed feedback loop that is defined by a specific time-delay and the so-called autaptic coupling strength. Recently, the role and function of autapses within the nervous system has been studied extensively. Here, we extend the scope of theoretical research by investigating the effects of an autapse on the transmission of a weak localized pacemaker activity in a scale-free neuronal network. Our results reveal that by mediating the spiking activity of the pacemaker neuron, an autapse increases the propagation of its rhythm across the whole network, if only the autaptic time delay and the autaptic coupling strength are properly adjusted. We show that the autapse-induced enhancement of the transmission of pacemaker activity occurs only when the autaptic time delay is close to an integer multiple of the intrinsic oscillation time of the neurons that form the network. In particular, we demonstrate the emergence of multiple resonances involving the weak signal, the intrinsic oscillations, and the time scale that is dictated by the autapse. Interestingly, we also show that the enhancement of the pacemaker rhythm across the network is the strongest if the degree of the pacemaker neuron is lowest. This is because the dissipation of the localized rhythm is contained to the few directly linked neurons, and only afterwards, through the secondary neurons, it propagates further. If the pacemaker neuron has a high degree, then its rhythm is simply too weak to excite all the neighboring neurons, and propagation therefore fails.展开更多
基金supported by the National Natural Science Foundation of China(Grant Nos.11325208&11572015)the Innovation Foundation of Beijing University of Aeronautics and Astronautics for PhD Graduates
文摘The study of synchronization and bursting transition is very important and valuable in cognitive activities and action control of brain as well as enhancement for the reliability of the cortex synapses. However, we wonder how the synaptic strength and synaptic delay, especially the asymmetrical time-delays between different neurons can collectively influence their synchronous firing behaviors. In this paper, based on the Hindmarsh-Rose neuronal systems with asymmetrical time-delays, we investigate the collective effects of various delays and coupling strengths on the synchronization and bursting transition. It is shown that the interplay between delay and coupling strength can not only enhance or destroy the synchronizations but also can induce the regular transitions of bursting firing patterns. Specifically, as the coupling strength or time-delay increasing, the firing patterns of the time-delayed coupling neuronal systems consistently present a regular transition, that is, the periods of spikes during the bursting firings increase firstly and then decrease slowly. In particular, in contrast to the case of symmetrical time-delays,asymmetrical time-delays can lead to the paroxysmal synchronizations of coupling neuronal systems, as well as the concentration level of synchronization for the non-identically coupled system is superior to the one of identical coupling. These results more comprehensively reveal the rich nonlinear dynamical behaviors of neuronal systems and may be helpful for us to have a better understanding of the neural coding.
文摘An autapse is an unusual synapse that occurs between the axon and the soma of the same neuron. Mathematically, it can be described as a self-delayed feedback loop that is defined by a specific time-delay and the so-called autaptic coupling strength. Recently, the role and function of autapses within the nervous system has been studied extensively. Here, we extend the scope of theoretical research by investigating the effects of an autapse on the transmission of a weak localized pacemaker activity in a scale-free neuronal network. Our results reveal that by mediating the spiking activity of the pacemaker neuron, an autapse increases the propagation of its rhythm across the whole network, if only the autaptic time delay and the autaptic coupling strength are properly adjusted. We show that the autapse-induced enhancement of the transmission of pacemaker activity occurs only when the autaptic time delay is close to an integer multiple of the intrinsic oscillation time of the neurons that form the network. In particular, we demonstrate the emergence of multiple resonances involving the weak signal, the intrinsic oscillations, and the time scale that is dictated by the autapse. Interestingly, we also show that the enhancement of the pacemaker rhythm across the network is the strongest if the degree of the pacemaker neuron is lowest. This is because the dissipation of the localized rhythm is contained to the few directly linked neurons, and only afterwards, through the secondary neurons, it propagates further. If the pacemaker neuron has a high degree, then its rhythm is simply too weak to excite all the neighboring neurons, and propagation therefore fails.
