Biology subjects

Pazienti, A.

Publications and source records attributed to Pazienti, A..

5 recordsLinked to original sources

bioRxiv2024

Circuit-Level Dynamics of Slow Wave Activity and Propagation During the Awakening Process

Slow-wave activity (SWA) is a hallmark of the loss of consciousness in non-REM sleep and anesthesia. The mechanistic underpinnings of SWA, and its evolution when transitioning towards the conscious brain state is poorly understood. We address this topic by recording multi-area and laminar activity in posterior parietal (PPC) and primary visual (V1) cortices of mice spontaneously awakening from isoflurane anesthesia. Spectral power is stronger in PPC (especially in superficial layers) during deep unconsciousness, but stronger in V1 when awakening. Rostro-caudal (feedback-like) propagation of SWA also shows state-dependent modulation, particularly in layer 5. The excitability of layer 2/3 neurons, hindered at high isoflurane, recovers during awakening, when V1 and the feedforward pathway reacquire a strong role. Detailing the hierarchical and laminar properties of spontaneous traveling oscillations, we provide evidence that SWA is a multiscale phenomenon. Explicating the functional role of these processes is critical to understand the neuronal mechanisms of consciousness.

neuroscience↗

bioRxiv2024

Probing the edge of synchronization: Slow waves erode resting activity in behaving monkeys

Brain networks oscillate between sleep and wakefulness, following circadian rhythms. Theoretical models suggest distinct phases within this cycle, separated by a critical point where long-range activity patterns emerge, an advantageous condition for information processing in cortical networks. However, the exact nature of this critical dynamics remains elusive. A key question is whether the brain operates at this critical point during cognitive tasks or only during resting wakefulness. Here, we analyzed neural signals from the premotor cortex (PMC) of two macaque monkeys engaged in a delayed-reaching task and under drug-induced unconsciousness. We found evidence of criticality during resting periods at the end of behavioral trials in the awake state. This scale-free activity appeared as coordinated traveling waves, like those observed during anesthesia. As predicted by spiking networks models, activity-dependent adaptation influences wave size, supporting the hypothesis that the PMC operates near a synchronization phase transition while avoiding it during active behaviors.

neuroscience↗

bioRxiv2021

Slow waves form expanding, memory-rich mesostates steered by local excitability in fading anesthesia

During sleep and anesthesia, large groups of neurons throughout the entire cortex activate rhythmically producing wavefronts of activity referred to as slow-wave activity (SWA). In the arousal process, the brain restores its integrative and complex activity. The network mechanisms underlying this global state transition remain however to be elucidated. Here we investigated the network features shaping the SWA under fading anesthesia. Using electrocorticographical recordings of wide cortical areas of the mouse brain, we developed a quantitative measure of the anesthesia level based on slow-wave frequency and complexity. At deep anesthesia, we document a stringent alternation of posterior-anterior-posterior modes of propagation. With fading anesthesia, SWA evolves to produce a plethora of metastable spatiotemporal patterns. A network model of spiking neurons reproduced the data using short-range connectivity, subcortical input and a local activity-dependent adaptation. The emergence from deep anesthesia does not require modifying the connectivity, but small changes in the local excitability of cortical cell assemblies, further supporting the hypothesis of a tight bound between scales in the brain.

neuroscience↗

bioRxiv2019

Modulation of coordinated activity across cortical layers by plasticity of inhibitory synapses onto layer 5 pyramidal neurons

In the neocortex, synaptic inhibition shapes all forms of spontaneous and sensory-evoked activity. Importantly, inhibitory transmission is highly plastic, but the functional role of inhibitory synaptic plasticity is unknown. In the mouse barrel cortex, activation of layer 2/3 PNs elicited strong feed-forward perisomatic inhibition (FFI) onto layer 5 PNs. We found that FFI involving PV cells was strongly potentiated by postsynaptic PN burst firing. FFI plasticity modified PN excitation-to-inhibition (E/I) ratio, strongly modulated PN gain and altered information transfer across cortical layers. Moreover, our LTPi-inducing protocol modified the firing of layer 5 PNs and altered the temporal association of PN spikes to {gamma}-oscillations both in vitro and in vivo. All these effects were captured by unbalancing the E/I ratio in a feed-forward inhibition circuit model. Altogether, our results indicate that activity-dependent modulation of perisomatic inhibitory strength effectively influences the participation of single principal cortical neurons to cognitive-relevant network activity.\n\nImpact StatementLong-term potentiation of feed-forward perisomatic inhibition effectively alters the computational properties of single layer 5 pyramidal neurons and their association to network activity.

neuroscience↗

bioRxiv2018

Strong preference for autaptic self-connectivity of neocortical PV interneurons entrains them to γ-oscillations

Parvalbumin (PV) positive interneurons modulate cortical activity through highly specialized connectivity patterns onto excitatory pyramidal neurons (PNs) and other inhibitory cells. PV cells are auto-connected through powerful autapses, but the contribution of this form of fast disinhibition to cortical function is unknown. We found that autaptic transmission represents the most powerful input of PV cells in neocortical Layer V. Autaptic strength was greater than synaptic strength onto PNs as result of a larger quantal size, whereas autaptic and heterosynaptic PV-PV synapses differed in the number of release sites. Overall, single-axon autaptic transmission contributed to ~40% of the total perisomatic inhibition that PV interneurons received. The strength of autaptic transmission modulated the coupling of PV-cell firing with optogenetically-induced {gamma}-oscillations preventing high frequency bursts of spikes. Autaptic self-inhibition represents an exceptionally large and fast disinhibitory mechanism to synchronize the output of PV cells during cognitive-relevant cortical network activity.

neuroscience↗