Biology subjects

Deleuze, C.

Publications and source records attributed to Deleuze, C..

5 recordsLinked to original sources

bioRxiv2026

Noradrenaline prolongs the state of motor arrest via cerebrospinal fluid signaling

Neuromodulators can mediate whole-body physiological changes, however how signaling from relatively small populations of neurons produces widespread and sustained effects remains incompletely understood. Here, we demonstrate that sustained noradrenergic activation induces prolonged motor arrest accompanied by postural collapse, bradycardia, and emetic responses. Motor suppression arises from inhibition of brainstem commands to the spinal cord rather than motoneuron silencing. Noradrenaline induces a glial calcium wave that propagates throughout the central nervous system. This wave most prominently persists at the brainstem-spinal cord boundary and ventricular midline. At this location, ependymal radial glia express Adra1a receptors on cilia contacting cerebrospinal fluid (CSF). Ventricular noradrenaline injections recapitulated the glial wave and motor arrest, while CSF administration of an Adra1 antagonist shortened motor arrest. Altogether, noradrenaline sustains motor arrest by signaling through the CSF via ciliary Adra1a receptors on ependymal radial glia showing that cerebrospinal fluid as a critical transmission route for persistence of behavioral states. HighlightsO_LINoradrenergic surges coordinate a whole-body response with motor arrest, postural disruptions, bradycardia, and emesis-like reflexes C_LIO_LIMotor arrest results from silencing of brainstem motor commands to the spinal cord C_LIO_LINoradrenaline-induced glial calcium waves last longest at the obex/ventricular midline where cilia of CSF-contacting glial cells bear Adra1 receptors C_LIO_LINoradrenergic signaling in the CSF is necessary and sufficient for motor arrest to persist C_LI

neuroscience↗

bioRxiv2020

A calibrated optogenetic toolbox of stable zebrafish opsin lines

Optogenetic actuators with diverse spectral tuning, ion selectivity and kinetics are constantly being engineered providing powerful tools for controlling neural activity with subcellular resolution and millisecond precision. Achieving reliable and interpretable in vivo optogenetic manipulations requires reproducible actuator expression and calibration of photocurrents in target neurons. Here, we developed nine transgenic zebrafish lines for stable opsin expression and calibrated their efficacy in vivo. We first used high-throughput behavioural assays to compare opsin ability to elicit or silence neural activity. Next, we performed in vivo whole-cell electrophysiological recordings to quantify the amplitude and kinetics of photocurrents and test opsin ability to precisely control spiking. We observed substantial variation in efficacy, associated with differences in both opsin expression level and photocurrent characteristics, and identified conditions for optimal use of the most efficient opsins. Overall, our calibrated optogenetic toolkit will facilitate the design of controlled optogenetic circuit manipulations.

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↗

bioRxiv2018

Perineuronal nets set the strength of thalamic recruitment of interneurons in the adult visual cortex

In the neocortex, the closure of critical periods (CPs) of plasticity is paralleled by the accumulation of perineuronal nets (PNNs) around parvalbumin (PV)-positive inhibitory interneurons. Accordingly, PNN degradation in adult mammals re-opens cortical plasticity. However, how PNNs tune cortical function and plasticity is unknown. We found that PNNs modulated the gain of visual responses in the adult mouse visual cortex in vivo. Removal of PNNs in adult V1 strongly increased thalamic neurotransmission selectively on layer 4 PV cells. This produced a differential gating of feed-forward inhibition on principal neurons and other PV cells, with no alterations of unitary inhibitory synaptic transmission and neuronal excitability. These effects depended on visual input, as they were strongly attenuated by monocular deprivation in PNN-depleted adult mice. Thus, PNNs control visual processing and plasticity by selectively setting the strength of thalamic recruitment of PV cells. We conclude that PNN accumulation during circuit maturation likely prevents excessive thalamic excitation of PV cells at the expense of cortical plasticity.

neuroscience↗