Publications by authors named "Bruno Delord"

Phasic variations in dopamine levels are interpreted as a teaching signal reinforcing rewarded behaviors. However, behavior also depends on the motivational, neuromodulatory effect of phasic dopamine. In this study, we reveal a neurodynamical principle that unifies these roles in a recurrent network-based decision architecture embodied through an action-perception loop with the task space, the MAGNet model.

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Cortical dynamics are organized over multiple anatomical and temporal scales. The mechanistic origin of the temporal organization and its contribution to cognition remain unknown. Here, we demonstrate the cause of this organization by studying a specific temporal signature (time constant and latency) of neural activity.

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In the prefrontal cortex (PFC), higher-order cognitive functions and adaptive flexible behaviors rely on continuous dynamical sequences of spiking activity that constitute neural trajectories in the state space of activity. Neural trajectories subserve diverse representations, from explicit mappings in physical spaces to generalized mappings in the task space, and up to complex abstract transformations such as working memory, decision-making and behavioral planning. Computational models have separately assessed learning and replay of neural trajectories, often using unrealistic learning rules or decoupling simulations for learning from replay.

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The ability to integrate information across time at multiple timescales is a vital element of adaptive behavior, because it provides the capacity to link events separated in time, extract useful information from previous events and actions, and to construct plans for behavior over time. Here we make the argument that this information integration capacity is a central function of the midcingulate cortex (MCC), by reviewing the anatomical, intrinsic network, neurophysiological, and behavioral properties of MCC. The MCC is the region of the medial wall situated dorsal to the corpus callosum and sometimes referred to as dACC.

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Action selection has been hypothesized to be a key function of the basal ganglia, yet the nuclei involved, their interactions and the importance of the direct/indirect pathway segregation in such process remain debated. Here, we design a spiking computational model of the monkey basal ganglia derived from a previously published population model, initially parameterized to reproduce electrophysiological activity at rest and to embody as much quantitative anatomical data as possible. As a particular feature, both models exhibit the strong overlap between the direct and indirect pathways that has been documented in non-human primates.

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Loss of function in the Scn1a gene leads to a severe epileptic encephalopathy called Dravet syndrome (DS). Reduced excitability in cortical inhibitory neurons is thought to be the major cause of DS seizures. Here, in contrast, we show enhanced excitability in thalamic inhibitory neurons that promotes the non-convulsive seizures that are a prominent yet poorly understood feature of DS.

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Persistent neural activity, the substrate of working memory, is thought to emerge from synaptic reverberation within recurrent networks. However, reverberation models do not robustly explain the fundamental dynamics of persistent activity, including high-spiking irregularity, large intertrial variability, and state transitions. While cellular bistability may contribute to persistent activity, its rigidity appears incompatible with persistent activity labile characteristics.

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Synaptic plasticity is a cardinal cellular mechanism for learning and memory. The endocannabinoid (eCB) system has emerged as a pivotal pathway for synaptic plasticity because of its widely characterized ability to depress synaptic transmission on short- and long-term scales. Recent reports indicate that eCBs also mediate potentiation of the synapse.

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Key Points: Although learning can arise from few or even a single trial, synaptic plasticity is commonly assessed under prolonged activation. Here, we explored the existence of rapid responsiveness of synaptic plasticity at corticostriatal synapses in a major synaptic learning rule, spike-timing-dependent plasticity (STDP). We found that spike-timing-dependent depression (tLTD) progressively disappears when the number of paired stimulations (below 50 pairings) is decreased whereas spike-timing-dependent potentiation (tLTP) displays a biphasic profile: tLTP is observed for 75-100 pairings, is absent for 25-50 pairings and re-emerges for 5-10 pairings.

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Homeostatic intrinsic plasticity (HIP) is a ubiquitous cellular mechanism regulating neuronal activity, cardinal for the proper functioning of nervous systems. In invertebrates, HIP is critical for orchestrating stereotyped activity patterns. The functional impact of HIP remains more obscure in vertebrate networks, where higher order cognitive processes rely on complex neural dynamics.

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Cerebrocortical injuries such as stroke are a major source of disability. Maladaptive consequences can result from post-injury local reorganization of cortical circuits. For example, epilepsy is a common sequela of cortical stroke, but the mechanisms responsible for seizures following cortical injuries remain unknown.

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Dendrites of cerebellar Purkinje cells (PCs) respond to brief excitations from parallel fibers with lasting plateau depolarizations. It is unknown whether these plateaus are local events that boost the synaptic signals or they propagate to the soma and directly take part in setting the cell firing dynamics. To address this issue, we analyzed a likely mechanism underlying plateaus in three representations of a reconstructed PC with increasing complexity.

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Synaptic plasticity is classically considered as the neuronal substrate for learning and memory. However, activity-dependent changes in neuronal intrinsic excitability have been reported in several learning-related brain regions, suggesting that intrinsic plasticity could also participate to information storage. Compared to synaptic plasticity, there has been little exploration of the properties of induction and expression of intrinsic plasticity in an intact brain.

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We present a mathematical analysis of the effects of Hebbian learning in random recurrent neural networks, with a generic Hebbian learning rule, including passive forgetting and different timescales, for neuronal activity and learning dynamics. Previous numerical work has reported that Hebbian learning drives the system from chaos to a steady state through a sequence of bifurcations. Here, we interpret these results mathematically and show that these effects, involving a complex coupling between neuronal dynamics and synaptic graph structure, can be analyzed using Jacobian matrices, which introduce both a structural and a dynamical point of view on neural network evolution.

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The aim of the present paper is to study the effects of Hebbian learning in random recurrent neural networks with biological connectivity, i.e. sparse connections and separate populations of excitatory and inhibitory neurons.

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Strong experimental evidence indicates that protein kinase and phosphatase (KP) cycles are critical to both the induction and maintenance of activity-dependent modifications in neurons. However, their contribution to information storage remains controversial, despite impressive modeling efforts. For instance, plasticity models based on KP cycles do not account for the maintenance of plastic modifications.

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Computational capabilities of Purkinje cells (PCs) are central to the cerebellum function. Information originating from the whole nervous system converges on their dendrites, and their axon is the sole output of the cerebellar cortex. PC dendrites respond to weak synaptic activation with long-lasting, low-amplitude plateau potentials, but stronger synaptic activation can generate fast, large amplitude calcium spikes.

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