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Register a new userOrder symmetry breaking and broad distribution of events in spiking neural networks with continuous membrane potential
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We introduce an exactly integrable version of the well-known leaky integrate-and-fire (LIF) model, with continuous membrane potential at the spiking event, the c-LIF. We investigate the dynamical regimes of a fully connected network of excitatory c-LIF neurons in the presence of short-term synaptic plasticity. By varying the coupling strength among neurons, we show that a complex chaotic dynamics arises, characterized by scale free avalanches. The origin of this phenomenon in the c-LIF can be related to the order symmetry breaking in neurons spike-times, which corresponds to the onset of a broad activity distribution. Our analysis uncovers a general mechanism through which networks of simple neurons can be attracted to a complex basin in the phase space.
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Curies principle states that when effects show certain asymmetry, this asymmetry must be found in the causes that gave rise to them. We demonstrate that symmetry equivariant neural networks uphold Curies principle and can be used to articulate many symmetry-relevant scientific questions into simple optimization problems. We prove these properties mathematically and demonstrate them numerically by training a Euclidean symmetry equivariant neural network to learn symmetry-breaking input to deform a square into a rectangle and to generate octahedra tilting patterns in perovskites.
Neuronal networks are controlled by a combination of the dynamics of individual neurons and the connectivity of the network that links them together. We study a minimal model of the preBotzinger complex, a small neuronal network that controls the breathing rhythm of mammals through periodic firing bursts. We show that the properties of a such a randomly connected network of identical excitatory neurons are fundamentally different from those of uniformly connected neuronal networks as described by mean-field theory. We show that (i) the connectivity properties of the networks determines the location of emergent pacemakers that trigger the firing bursts and (ii) that the collective desensitization that terminates the firing bursts is determined again by the network connectivity, through k-core clusters of neurons.
In this paper, we clarify the mechanisms underlying a general phenomenon present in pulse-coupled heterogeneous inhibitory networks: inhibition can induce not only suppression of the neural activity, as expected, but it can also promote neural reactivation. In particular, for globally coupled systems, the number of firing neurons monotonically reduces upon increasing the strength of inhibition (neurons death). However, the random pruning of the connections is able to reverse the action of inhibition, i.e. in a sparse network a sufficiently strong synaptic strength can surprisingly promote, rather than depress, the activity of the neurons (neurons rebirth). Thus the number of firing neurons reveals a minimum at some intermediate synaptic strength. We show that this minimum signals a transition from a regime dominated by the neurons with higher firing activity to a phase where all neurons are effectively sub-threshold and their irregular firing is driven by current fluctuations. We explain the origin of the transition by deriving an analytic mean field formulation of the problem able to provide the fraction of active neurons as well as the first two moments of their firing statistics. The introduction of a synaptic time scale does not modify the main aspects of the reported phenomenon. However, for sufficiently slow synapses the transition becomes dramatic, the system passes from a perfectly regular evolution to an irregular bursting dynamics. In this latter regime the model provides predictions consistent with experimental findings for a specific class of neurons, namely the medium spiny neurons in the striatum.
We consider two neuronal networks coupled by long-range excitatory interactions. Oscillations in the gamma frequency band are generated within each network by local inhibition. When long-range excitation is weak, these oscillations phase-lock with a phase-shift dependent on the strength of local inhibition. Increasing the strength of long-range excitation induces a transition to chaos via period-doubling or quasi-periodic scenarios. In the chaotic regime oscillatory activity undergoes fast temporal decorrelation. The generality of these dynamical properties is assessed in firing-rate models as well as in large networks of conductance-based neurons.
Experimental and numerical results suggest that the brain can be viewed as a system acting close to a critical point, as confirmed by scale-free distributions of relevant quantities in a variety of different systems and models. Less attention has received the investigation of the temporal correlation functions in brain activity in different, healthy and pathological, conditions. Here we perform this analysis by means of a model with short and long-term plasticity which implements the novel feature of different recovery rates for excitatory and inhibitory neurons, found experimentally. We evidence the important role played by inhibitory neurons in the supercritical state: We detect an unexpected oscillatory behaviour of the correlation decay, whose frequency depends on the fraction of inhibitory neurons and their connectivity degree. This behaviour can be rationalized by the observation that bursts in activity become more frequent and with a smaller amplitude as inhibition becomes more relevant.
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