Taken together, the findings show consistent neural aberrations during reward processing in depression, namely, reduced striatal signal during feedback and blunted FRN. These aberrations may underlie the pathogenesis of depression and have important implications for development of new treatments.

Humans refer to their mood state regularly in day-to-day as well as clinical interactions. Theoretical accounts suggest that when reporting on our mood we integrate over the history of our experiences; yet, the temporal structure of this integration remains unexamined. Here we use a computational approach to quantitatively answer this question and show that early events exert a stronger influence on reported mood compared to recent events. We show that a Primacy model accounts better for mood reports compared to a range of alternative temporal representations across random, consistent or dynamic reward environments, different age groups and in both healthy and depressed participants. Moreover, we find evidence for neural encoding of the Primacy, but not the Recency, model in frontal brain regions related to mood regulation. These findings hold implications for the timing of events in experimental or clinical settings and suggest new directions for individualized mood interventions.

In recent years much effort is invested in means to control neural population responses at the whole brain level, within the context of developing advanced medical applications. The tradeoffs and constraints involved, however, remain elusive due to obvious complications entailed by studying whole brain dynamics. Here, we present effective control of response features (probability and latency) of cortical networks in vitro over many hours, and offer this approach as an experimental toy for studying controllability of neural networks in the wider context. Exercising this approach we show that enforcement of stable high activity rates by means of closed loop control may enhance alteration of underlying global input–output relations and activity dependent dispersion of neuronal pair-wise correlations across the network.

Both human and animal studies support the relationship between depression and reward processing abnormalities, giving rise to the expectation that neural signals of these processes may serve as biomarkers or mechanistic treatment targets. Given the great promise of this research line, we scrutinized those findings and the theoretical claims that underlie them. To achieve this, we applied the framework provided by classical work on causality as well as contemporary approaches to prediction. We identified a number of conceptual, practical, and analytical challenges to this line of research and used a preregistered meta-analysis to quantify the longitudinal associations between reward processing abnormalities and depression. We also investigated the impact of measurement error on reported data. We found that reward processing abnormalities do not reach levels that would be useful for clinical prediction, yet the available evidence does not preclude a possible causal role in depression.

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Developing technologies for coupling neural activity and artificial neural components, is key for advancing neural interfaces and neuroprosthetics. We present a biohybrid experimental setting, where the activity of a biological neural network is coupled to a biomimetic hardware network. The implementation of the hardware network (denoted NeuroSoC) exhibits complex dynamics with a multiplicity of time-scales, emulating 2880 neurons and 12.7 M synapses, designed on a VLSI chip. This network is coupled to a neural network in vitro , where the activities of both the biological and the hardware networks can be recorded, processed, and integrated bidirectionally in real-time. This experimental setup enables an adjustable and well-monitored coupling, while providing access to key functional features of neural networks. We demonstrate the feasibility to functionally couple the two networks and to implement control circuits to modify the biohybrid activity. Overall, we provide an experimental model for neuromorphic-neural interfaces, hopefully to advance the capability to interface with neural activity, and with its irregularities in pathology.

Neural synchronization across long distances is a functionally important phenomenon in health and disease. In order to access the basis of different modes of long-range synchrony, we monitor spiking activities over centimetre scale in cortical networks and show that the mode of synchrony depends upon a length scale, λ, which is the minimal path that activity should propagate through to find its point of origin ready for reactivation. When λ is larger than the physical dimension of the network, distant neuronal populations operate synchronously, giving rise to irregularly occurring network-wide events that last hundreds of milliseconds to several seconds. In contrast, when λ approaches the dimension of the network, a continuous self-sustained reentry propagation emerges, a regular seizure-like mode that is marked by precise spatiotemporal patterns (‘synfire chains’) and may last many minutes. Termination of a reentry phase is preceded by a decrease of propagation speed to a halt. Stimulation decreases both propagation speed and λ values, which modifies the synchrony mode respectively. The results contribute to the understanding of the origin and termination of different modes of neural synchrony as well as their long-range spatial patterns, while hopefully catering to manipulation of the phenomena in pathological conditions.

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