Integrated information decomposition unveils major structural traits of in silico and in vitro neuronal networks.

The properties of complex networked systems arise from the interplay between the dynamics of their elements and the underlying topology. Thus, to understand their behavior, it is crucial to convene as much information as possible about their topological organization. However, in large systems, such as neuronal networks, the reconstruction of such topology is usually carried out from the information encoded in the dynamics on the network, such as spike train time series, and by measuring the transfer entropy between system elements. The topological information recovered by these methods does not necessarily capture the connectivity layout, but rather the causal flow of information between elements. New theoretical frameworks, such as Integrated Information Decomposition (Φ-ID), allow one to explore the modes in which information can flow between parts of a system, opening a rich landscape of interactions between network topology, dynamics, and information. Here, we apply Φ-ID on in silico and in vitro data to decompose the usual transfer entropy measure into different modes of information transfer, namely, synergistic, redundant, or unique. We demonstrate that the unique information transfer is the most relevant measure to uncover structural topological details from network activity data, while redundant information only introduces residual information for this application. Although the retrieved network connectivity is still functional, it captures more details of the underlying structural topology by avoiding to take into account emergent high-order interactions and information redundancy between elements, which are important for the functional behavior, but mask the detection of direct simple interactions between elements constituted by the structural network topology.

Frequency Selectivity of Neural Circuits With Heterogeneous Discrete Transmission Delays.

Neurons are connected to other neurons by axons and dendrites that conduct signals with finite velocities, resulting in delays between the firing of a neuron and the arrival of the resultant impulse at other neurons. Since delays greatly complicate the analytical treatment and interpretation of models, they are usually neglected or taken to be uniform, leading to a lack in the comprehension of the effects of delays in neural systems. This letter shows that heterogeneous transmission delays make small groups of neurons respond selectively to inputs with differing frequency spectra. By studying a single integrate-and-fire neuron receiving correlated time-shifted inputs, it is shown how the frequency response is linked to both the strengths and delay times of the afferent connections. The results show that incorporating delays alters the functioning of neural networks, and changes the effect that neural connections and synaptic strengths have.

A calcium-influx-dependent plasticity model exhibiting multiple STDP curves.

Hebbian plasticity means that if the firing of two neurons is correlated, then their connection is strengthened. Conversely, uncorrelated firing causes a decrease in synaptic strength. Spike-timing-dependent plasticity (STDP) represents one instantiation of Hebbian plasticity. Under STDP, synaptic changes depend on the relative timing of the pre- and post-synaptic firing. By inducing pre- and post-synaptic firing at different relative times the STDP curves of many neurons have been determined, and it has been found that there are different curves for different neuron types or synaptic sites. Biophysically, strengthening (long-term potentiation, LTP) or weakening (long-term depression, LTD) of glutamatergic synapses depends on the post-synaptic influx of calcium (Ca2+): weak influx leads to LTD, while strong, transient influx causes LTP. The voltage-dependent NMDA receptors are the main source of Ca2+ influx, but they will only open if a post-synaptic depolarisation coincides with pre-synaptic neurotransmitter release. Here we present a computational mechanism for Ca2+-dependent plasticity in which the interplay between the pre-synaptic neurotransmitter release and the post-synaptic membrane potential leads to distinct Ca2+ time-courses, which in turn lead to the change in synaptic strength. It is shown that the model complies with classic STDP results, as well as with results obtained with triplets of spikes. Furthermore, the model is capable of displaying different shapes of STDP curves, as observed in different experimental studies.

Rich dynamics and functional organization on topographically designed neuronal networks in vitro.

Neuronal cultures are a prominent experimental tool to understand complex functional organization in neuronal assemblies. However, neurons grown on flat surfaces exhibit a strongly coherent bursting behavior with limited functionality. To approach the functional richness of naturally formed neuronal circuits, here we studied neuronal networks grown on polydimethylsiloxane (PDMS) topographical patterns shaped as either parallel tracks or square valleys. We followed the evolution of spontaneous activity in these cultures along 20 days in vitro using fluorescence calcium imaging. The networks were characterized by rich spatiotemporal activity patterns that comprised from small regions of the culture to its whole extent. Effective connectivity analysis revealed the emergence of spatially compact functional modules that were associated with both the underpinned topographical features and predominant spatiotemporal activity fronts. Our results show the capacity of spatial constraints to mold activity and functional organization, bringing new opportunities to comprehend the structure-function relationship in living neuronal circuits.