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Authors
Dietmar Plenz
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It is shown that, contrary to the claims in a recent letter by Haldeman and Beggs (PRL, 94, 058101, 2005), the branching ratio in epileptic cortical cultures is smaller than one. In addition, and also in contrast to claims made in that paper, the number of metastable states is not significantly different between cortical cultures in the critical state and cultures made epileptic using picrotoxin.
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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.
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.
We model spontaneous cortical activity with a network of coupled spiking units, in which multiple spatio-temporal patterns are stored as dynamical attractors. We introduce an order parameter, which measures the overlap (similarity) between the activity of the network and the stored patterns. We find that, depending on the excitability of the network, different working regimes are possible. For high excitability, the dynamical attractors are stable, and a collective activity that replays one of the stored patterns emerges spontaneously, while for low excitability, no replay is induced. Between these two regimes, there is a critical region in which the dynamical attractors are unstable, and intermittent short replays are induced by noise. At the critical spiking threshold, the order parameter goes from zero to one, and its fluctuations are maximized, as expected for a phase transition (and as observed in recent experimental results in the brain). Notably, in this critical region, the avalanche size and duration distributions follow power laws. Critical exponents are consistent with a scaling relationship observed recently in neural avalanches measurements. In conclusion, our simple model suggests that avalanche power laws in cortical spontaneous activity may be the effect of a network at the critical point between the replay and non-replay of spatio-temporal patterns.
We consider a sparse random network of excitatory leaky integrate-and-fire neurons with short-term synaptic depression. Furthermore to mimic the dynamics of a brain circuit in its first stages of development we introduce for each neuron correlations among in-degree and out-degree as well as among excitability and the corresponding total degree, We analyze the influence of single neuron stimulation and deletion on the collective dynamics of the network. We show the existence of a small group of neurons capable of controlling and even silencing the bursting activity of the network. These neurons form a functional clique since only their activation in a precise order and within specific time windows is capable to ignite population bursts.
We study the storage of multiple phase-coded patterns as stable dynamical attractors in recurrent neural networks with sparse connectivity. To determine the synaptic strength of existent connections and store the phase-coded patterns, we introduce a learning rule inspired to the spike-timing dependent plasticity (STDP). We find that, after learning, the spontaneous dynamics of the network replay one of the stored dynamical patterns, depending on the network initialization. We study the network capacity as a function of topology, and find that a small- world-like topology may be optimal, as a compromise between the high wiring cost of long range connections and the capacity increase.
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