Abstract
In the brain, synchronization among cells of an assembly is a common phenomenon, and thought to be functionally relevant. Here we used an in vitro experimental model of cell assemblies, cortical cultures, combined with numerical simulations of a spiking neural network (SNN) to investigate how and why spontaneous synchronization occurs. In order to deal with excitation only, we pharmacologically blocked GABAAergic transmission using bicuculline. Synchronous events in cortical cultures tend to involve almost every cell and to display relatively constant durations. We have thus named these “network spikes” (NS). The inter-NS-intervals (INSIs) proved to be a more interesting phenomenon. In most cortical cultures NSs typically come in series or bursts (“bursts of NSs”, BNS), with short (∼1 s) INSIs and separated by long silent intervals (tens of s), which leads to bimodal INSI distributions. This suggests that a facilitating mechanism is at work, presumably short-term synaptic facilitation, as well as two fatigue mechanisms: one with a short timescale, presumably short-term synaptic depression, and another one with a longer timescale, presumably cellular adaptation. We thus incorporated these three mechanisms into the SNN, which, indeed, produced realistic BNSs. Next, we systematically varied the recurrent excitation for various adaptation timescales. Strong excitability led to frequent, quasi-periodic BNSs (CV∼0), and weak excitability led to rare BNSs, approaching a Poisson process (CV∼1). Experimental cultures appear to operate within an intermediate weakly-synchronized regime (CV∼0.5), with an adaptation timescale in the 2–8 s range, and well described by a Poisson-with-refractory-period model. Taken together, our results demonstrate that the INSI statistics are indeed informative: they allowed us to infer the mechanisms at work, and many parameters that we cannot access experimentally.
Highlights
It is well known that dissociated cultured neuronal networks display spontaneous activity
Other authors have focused on INSI distribution-tails, which has led to controversial results with evidence for both scale-free distributed
As we will see in the Result section, the mechanism that we propose for BNS requires that tDvtF, as found in ref
Summary
It is well known that dissociated cultured neuronal networks display spontaneous activity. This activity is not steady but shows instead brief periods (0.1–0.2 s) during which most of the neurons burst – a phenomenon called ‘‘network spikes’’ (NS) – separated by almost silent intervals lasting several seconds [1,2,3,4,5,6,7,8,9,10,11]. It has been shown that typical NS’ rise time is shorter when GABAA receptors are blocked [4]. Typical time courses suggest the presence of ‘‘pacemaker’’ neurons and adaptive synapses [9]. Other authors have focused on INSI distribution-tails, which has led to controversial results with evidence for both scale-free distributed
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