Biology subjects

Rouach, N.

Publications and source records attributed to Rouach, N..

At least 19 recordsLinked to original sources

bioRxiv2026

Synergistic effects of presynaptic and postsynaptic neurons give rise to three-stage short-term plasticity in vivo

Short-term plasticity (STP) is the transient fluctuation of connection strength between two neurons depending on the recent history of neuronal activity. STP shapes neurotransmission over time and plays important roles in circuit computations. It is classically quantified ex vivo either at the synaptic level or at the level of spike transmission from the presynaptic neuron to the postsynaptic neuron. However, the exact relationship between the postsynaptic dendritic responses and spike transmission during STP still remains unclear in vivo. Here, we characterized together the STP of both postsynaptic dendritic responses, measured by the postsynaptic field potential (PFP), and spike transmission at the retinocollicular pathway of mice. We found mostly facilitating STP, where the second presynaptic spike occurring within 25 ms induces a larger PFP, and consequently a higher postsynaptic firing rate compared to responses from the first presynaptic spike. Both PFP and spike transmission exhibit short-term facilitation, but to a different degree, where the facilitation in the spike transmission is larger than the PFP. The PFP and spike transmission also exhibit facilitation of different decay time constants, indicating a nonlinear relationship between the two. Interestingly, a preceding postsynaptic spike can induce a similarly large but longer lasting facilitation on the spike transmission upon receiving a subsequent presynaptic input. However, STP of the PFP does not depend on the preceding postsynaptic spike, suggesting that this longer postsynaptic facilitation has a nonsynaptic origin. Overall, our results indicate that STP of the retinocollicular pathway exhibits three different stages: 1) a weak synaptic facilitation of postsynaptic dendritic responses, 2) a strong synaptic facilitation of spike transmission, and 3) a longer lasting nonsynaptic facilitation of spike transmission. Using a computational model, we show that the second STP stage is a direct inheritance from the first STP stage, whereas two opposing nonsynaptic mechanisms with different time constants are needed for the emergence of the third STP stage. These findings provide direct evidence that synaptic and nonsynaptic STPs coexist in vivo, paving the way for large-scale measurement of these STPs and offering a means to monitor the transmission of information in neural circuits of behaving animals.

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bioRxiv2026

Sharp and Fast Dynamic Extraction and Tracking of Emitted Cellular Transients

Genetically encoded fluorescent sensors have expanded our ability to image cellular activity and transmitter release. Yet, sparse and low-salience events remain difficult to resolve against complex and fluctuating fluorescence backgrounds. Here we introduce DETECT, Dynamic Extraction and Tracking of Emitted Cellular Transients, which combines adaptive background suppression, probabilistic classification and multi-object tracking to extract fluorescence events while preserving their identity. Across synthetic datasets, DETECT improved detection and segmentation accuracy and reduced computational cost relative to established event-based methods. We validated DETECT across confocal, two-photon and miniscope imaging, ex vivo and in vivo, using calcium indicators and monoamine sensors. Beyond its technical performance, DETECT extends event-based analysis to low-salience fluorescence signals while resolving events spanning broad ranges of amplitude, morphology and dynamics. By resolving spontaneous dopamine and noradrenaline signals as distinct, trackable release events, DETECT reveals the spatiotemporal organization of neuromodulatory activity and provides a broadly applicable approach to quantitative fluorescence analysis.

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bioRxiv2026

Synaptic Input Triggers On-Demand Spine-Specific Mitochondrial ATP Production and Delivery

Synaptic activity imposes acute energy demands, especially for restoring ionic gradients via pumps and exchangers that require ATP. While mitochondria are positioned near dendritic spines to meet this demand, how ATP is produced and delivered with spatial precision remains unclear. Here, using high-resolution calcium and ATP imaging, immuno-cytochemistry, and computational modeling, we demonstrate that synaptic input--but not back-propagating action potentials (bAPs)--triggers on-demand mitochondrial ATP production. This occurs only in spines containing a spine apparatus (SA), where calcium-induced calcium release (CICR) activates mitochondrial calcium uniporters (MCUs), initiating ATP synthesis. We show that ATP delivery is spatially constrained to mitochondrial regions facing the spine base, where ATP-synthase is enriched. Importantly, ATP produced elsewhere on the mitochondrial surface tends to diffuse into the dendrite. We further demonstrate that the delivery of ATP to the spine head is geometrically optimized: an intermediate spine neck length maximizes delivery efficiency. Mathematical modeling and simulations revealb that the time scale for ATP to reach and refill all head-localized exchangers is on the order of hundreds of milliseconds--fast enough to meet local metabolic needs. The present findings establish a mechanism in which nanoscale calcium signaling and mitochondrial architecture together ensure rapid, spatially targeted ATP delivery, tightly coupled to synaptic activity.

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bioRxiv2026

Long-projection astrocytes challenge canonical territorial organization in the sleep-promoting VLPO

The ventrolateral preoptic nucleus (VLPO) is a key hypothalamic hub for non-rapid eye movement sleep, yet the glial architecture supporting its circuits remains poorly understood. Here, combining genetic labeling, high-resolution imaging and calcium imaging, we uncover unexpected astrocyte diversity in the VLPO. In addition to classical protoplasmic astrocytes, we identify paired "doublet" astrocytes associated with high local proliferative activity, as revealed by EdU incorporation. We further describe a population of long-projection astrocytes extending processes far beyond canonical astrocytic territories and contacting distant cells. These projections challenge the classical territorial organization of astrocytes and resemble morphologies previously thought to be restricted to hominid brains. Notably, VLPO astrocytes display robust spontaneous Ca{superscript 2} activity and a highly functionally connected network compared to astrocytes in the cortex and hippocampus. Together, these findings reveal specialized astrocyte architectures and enhanced glial network integration within a sleep-promoting nucleus. Reporting summaryBellier et al. identify three astrocyte subtypes in the sleep-promoting VLPO, including long-projection astrocytes with hominid-like morphology. They uncover marked postnatal gliogenesis, distinctive spontaneous Ca{superscript 2} dynamics, and tightly interconnected astrocytic networks, revealing region-specific astrocyte specialization and enhanced glial communication.

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bioRxiv2026

Astrocytes control oxytocin-based maternal behavior via connexin 30

Prosocial and affiliative behaviors rely on complex neuroendocrine neuronal circuits. Dynamic neuroglial interactions play prominent roles in shaping synaptic networks, whose alterations contribute to psychiatric disorders associated with social deficits. However, a role for astrocytes in regulating maternal behavior remains elusive. Here we show that female mice exhibiting increased oxytocin levels in the hypothalamic supraoptic nucleus upon social interactions with pups display neuroglial structural plasticity and downregulation of astroglial connexin 30, a protein involved in morphological remodeling. We found that impairing astroglial connexin 30 expression alters the structural properties of astrocytes by decreasing their volume and coverage of oxytocinergic synapses in the supraoptic nucleus of female mice. This functionally sets levels of plasma oxytocin and maternal behavior, exacerbating maternal care in virgin pup-naive female mice deficient for astroglial Cx30. Hypothalamic astrocytes, via connexin 30, are thus key determinants of oxytocin-based maternal behavior, whose alteration is known to impair social skills development in offspring.

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bioRxiv2025

Thalamocortical coupling and cortical E-I balance generate diverse anesthetic α-spindles for interpretable EEG decoding

The neuronal circuits generating frequency (8-13Hz) oscillatory patterns during anesthesia are poorly understood, making their use difficult in predictive medicine. Here, we combine large-scale in vivo recordings of thalamocortical neuronal ensembles in anesthetized mice with a minimal neural mass model. We report non-rhythmic, weakly synchronized firing of thalamic and cortical neurons correlated with oscillatory patterns, indicating an emergent network rather than cellular dynamics. The associated imbalance between the firing of excitatory and inhibitory cortical neurons, together with an increase in firing fluctuations, favors larger amplitudes oscillations, whereas changes in thalamic neuron output control oscillation frequency. A neural mass model, comprising reciprocally connected excitatory and inhibitory cortical and thalamic neurons well reproduces the oscillation patterns observed in vivo at increasing anesthetic doses. These results provide a direct link between EEG oscillations during anesthesia and their underlying network/cellular dynamics which are well captured by a computational model that is clinically relevant for anesthetized brain state monitoring. HighlightsO_LI transient patterns during anesthesia emerge from thalamocortical and cortical excitatory-inhibitory (E-I) network dynamics. C_LIO_LI pattern frequency and amplitude reflect depth of anesthesia, dynamic thalamocortical equilibrium and E-I imbalance. C_LIO_LIEmergence of spindle-like patterns at multiple frequency defines newly characterized brain-state during anesthesia C_LIO_LIA mass-model reproduces the transient nature and spectral diversity of anesthetic-induced oscillations, linking neural circuit mechanisms to EEG output. C_LI

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bioRxiv2025

Mapping glioblastoma spreading: connexin43 and glial dynamic in mouse and human glioblastoma microenvironment

High-grade gliomas (HGGs), including astrocytoma and glioblastoma (GBM), constitute the most prevalent primary tumors of the central nervous system (CNS). GBM cells demonstrate a notable ability to infiltrate the brain parenchyma, precluding complete surgical resection. Here we investigated the spreading of GBM cells and the response of the CNS microenvironment focusing on glial cells, which are essential interactors to GBM. We used acute and organotypic slices from the mouse brain and peritumoral cortex of patients with HGGs. We found that human peritumoral tissue from cortical resection was characterized by high levels of the astrocytic Connexin43 protein (Cx43) and discrete infiltration of microglia. In contrast, the tumor core exhibited high myeloid infiltration and an altered extracellular matrix (ECM) composition, which was poor in CD44. We tracked mouse and primary human-labeled-GBM cells in 2D cultures and in co-culture with organotypic slices generated from mouse brain and human peritumoral tissues. We found that the implanted GBM cells infiltrated the brain tissue, implying early glial modifications including an increase in Cx43 expression and distribution. Furthermore, the blockage of Cx43 hemichannels was accompanied by morphological changes and polarization of human GBM cells, typical for migration phenomena. The present study sheds light on the dynamics of GBM cells spreading in the living brain tissue, suggesting that the progression of the tumor correlates with changes within the host brain. Our findings identify the upregulation of Cx43 expression as a highly consistent modification in both mouse and human tissue that may be crucial for GBM infiltration.

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bioRxiv2025

Slow Intrinsic Oscillations in the Ventrolateral Preoptic nucleus

The ventrolateral preoptic nucleus (VLPO) of the hypothalamus plays a major role in the induction and consolidation of non-rapid eye movement (NREM) sleep. While VLPO neurons are heterogeneous, they often display low-threshold spikes (LTS), a feature that supports rhythmic activity. Nevertheless, rhythmic bursting in these VLPO neurons has never been observed. Here, we report that [~]12% of VLPO neurons in a large database of ex vivo patch-clamp recordings display spontaneous rhythmic bursting of action potentials. This activity occurred in putative sleep-promoting neurons, identified by inhibitory responses to noradrenaline (NA), as well as wake-active neurons that were activated by NA. Unsupervised clustering of 24 neurons based on burst properties, electrophysiological, and morphological features revealed three distinct groups: one corresponding to putative sleep-promoting neurons and two wake-active neurons with fast and slow bursting dynamics. Strikingly, membrane potential oscillations persisted in the presence of tetrodotoxin (TTX), indicating that rhythmic bursting is driven by intrinsic mechanisms rather than network activity. These findings suggest that rhythmic bursting is an intrinsic and functionally relevant mode of activity in VLPO neurons, which may contribute to sleep regulation.

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bioRxiv2025

Astroglial deficiency for oligophrenin-1 contributes to intellectual disability

Neurodevelopmental disorders, including X-linked intellectual disability, autism spectrum disorder or schizophrenia, can result from the mutation of oligophrenin-1 (Ophn1), encoding a Rho-GTPase-activating protein. Ophn1 regulates synaptic development and function, in part via cytoskeleton reorganization, and is expressed in both neurons and astrocytes. Despite the crucial role of astrocytes in synapse function, altered in neurodevelopmental disorders, and their Ophn1 expression, the specific impact of astroglial Ophn1 deficiency on synaptic transmission and behavior remains unknown. Here, we show that Ophn1 deficiency postnatally in hippocampal astrocytes impairs synaptic transmission, short-term plasticity and spatial working memory in adults. This involves an adenosine A1 receptor-dependent presynaptic mechanism associated with astroglial morphological rearrangements resulting in increased astroglial synapse coverage. The structural, functional and behavioral alterations induced by astroglial Ophn1 deficiency are rescued in adults by pharmacological inhibition of the RhoA/ROCK pathway. Our findings uncover an important role for astroglial Ophn1 deficiency in synaptic and behavioral dysfunctions, pointing to a novel cellular therapeutic target for neurodevelopmental disorders.

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bioRxiv2024

Unveiling the Functional Connectivity of Astrocytic Networks with AstroNet, a Graph Reconstruction Algorithm Coupled to Image Processing

Astrocytes form extended intercellular networks, displaying complex calcium activity. However, the specific organization of these astrocytic networks and the precise extent of their functional connectivity in different brain areas remain unexplored. To unveil the functional architecture of astrocytic networks, we developed, using a data-driven methodology, a novel algorithm called AstroNet that uses two-photon calcium imaging to map temporal correlations in activation events among neighboring astro-cytes. Our approach involves reconstructing functional astrocytic networks by organizing individual astrocyte activation events chronologically. This chronological order creates activity paths that enable the extraction of local astrocyte functional correlations. Ultimately, by tallying the occurrences of direct co-activations between pairs of cells along these pathways, we construct a graph that mirrors the underlying astrocyte functional network. By applying this method to two distinct brain regions (CA1 hippocampus and motor cortex), we identified notable differences in local network organizations in sub-regions of around 20-40 astrocytes. Specifically, the cortex exhibited a lower connectivity, while astrocytes in the hippocampus displayed stronger connections. Moreover, we found that in both regions, astrocytic networks consist of smaller, tightly connected sub-networks embedded within a larger, more loosely connected one. Altogether, our innovative method enables the identification of activation paths among astrocytes, facilitates the characterization of local network functional connectivity, and quantifies distinct connectivity patterns among astrocytes from different brain regions. This approach sheds light on the heterogeneous functional organization of astrocytic networks within the brain, pointing to region-specific astrocyte connectivity.

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bioRxiv2024

Functional contribution of astrocytic Kir4.1 channels to spasticity after spinal cord injury

Spasticity, a prevalent motor issue characterized by network hyperexcitability, causes pain and discomfort, with existing treatments offering limited relief. While past research has focused on neuronal factors, the role of astrocytes in spasticity has been overlooked. This study explores the potential of restoring astrocytic potassium (K+) uptake to reduce spasticity following SCI. Astrocytes buffer extracellular K+ via Kir4.1 channels, preventing neuronal hyperexcitability. Following spinal cord injury (SCI), Kir4.1 levels decrease at the injury site, though the consequences and mechanisms of this reduction within the motor output area have not been investigated. Utilizing advanced techniques, we demonstrate that lumbar astrocytes in a juvenile thoracic SCI mouse model switch to reactive phenotype, displaying morpho-functional and pro-inflammatory changes. These astrocytes also experience NBCe1-mediated intracellular acidosis, leading to Kir4.1 dysfunction and impaired K+ uptake. Enhancing Kir4.1 function reduces spasticity in SCI mice, revealing new therapeutic targets for neurological diseases associated with neuronal hyperexcitability. HighlightsO_LILumbar astrocytes adopt a reactive phenotype following a thoracic SCI C_LIO_LINBCe1-mediated acidosis in astrocytes disrupts Kir4.1 function post-SCI. C_LIO_LIImpaired K+ uptake leads to motoneuron hyperexcitability post-SCI. C_LIO_LIEnhanced astroglial Kir4.1 function reduces spastic-like symptoms in SCI mice. C_LI

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bioRxiv2024

Oxytocin Gαi signaling-induced amygdala astrocytes processes retraction shapes behavioral stress response

Anticipated reactions to stressful situations are vital for the survival and well-being of organisms, and abnormal reactions are involved in stress-related disorders. The neuropeptide oxytocin is a key modulator ensuring well-adapted stress responses. Oxytocin acts on both neurons and astrocytes, but the molecular and cellular mechanisms mediating stress response remain poorly understood. Here, we focus on the amygdala, a crucial hub that integrates and processes sensory information through oxytocin- dependent mechanisms. Using an acute stress paradigm in mice, genetic and pharmacological manipulations combined with proteomic, morphological, electrophysiological and behavioral approaches, we reveal that oxytocinergic modulation of the freezing response to stress is mediated by transient Gi-dependent retraction of astrocytic processes, followed by enhanced neuronal sensitivity to extracellular potassium in the amygdala. Our findings elucidate a pivotal role for astrocytes morphology- dependent modulation of brain circuits that is required for proper anticipated behavioral response to stressful situations.

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bioRxiv2024

Differential Short-Term Facilitation Of Synaptic Inputs And Spike Transmission At The Retinocollicular Synapse In Vivo

Short-term plasticity (STP) is important for understanding how neuronal circuits can perform different computations. The STP of a neuron pair can be measured directly using paired whole-cell recordings. Besides, the cross-correlation between the presynaptic and postsynaptic neuronal firing is usually used as a proxy for estimating the synaptic properties. However, the relationships between the synaptic inputs and the spiking properties of the postsynaptic neurons during the STP in vivo still remain unclear. Here, we characterized the STP of both synaptic input, measured by the postsynaptic field potential (PFP), and spike transmission at the retinocollicular pathway of mice. We found that the STP of the retinocollicular pathway is mainly facilitating, where the second presynaptic spike induces a larger PFP and higher postsynaptic firing rate than the first presynaptic spike. The facilitation in the postsynaptic firing rate is generally larger than the PFP facilitation. Interestingly, the last postsynaptic spike timing also has a large facilitating effect on the postsynaptic spiking upon receiving a presynaptic input spike. However, the PFP does not depend on the last postsynaptic spike timing, suggesting that there is an input-independent component of spike transmission in STP. Overall, our results indicate that the STP of the retinocollicular pathway is likely a two-stage process, where the spiking plasticity of the postsynaptic neuron could be independent of its inputs. HighlightsO_LIMeasure the short-term plasticity of the postsynaptic dendritic response and the spike transmission simultaneously C_LIO_LIThe retinocollicular pathway exhibits paired-spike facilitation C_LIO_LISpike transmission facilitates more than postsynaptic dendritic response C_LIO_LIShort last postsynaptic spike time facilitates spike transmission independent of the next presynaptic input C_LI

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bioRxiv2022

Astroglial gap junctions strengthen hippocampal network activity by sustaining afterhyperpolarization via KCNQ channels

Throughout the brain, astrocytes form networks mediated by gap-junction channels that promote the activity of neuronal ensembles. Although their inputs on neuronal information processing are well established, how molecularly gap junction channels shape neuronal network patterns remains unclear. Here using astroglial connexin-deficient mice, in which astrocytes are disconnected and neuronal bursting patterns are abnormal, we found that astrocyte networks strengthen bursting activity via dynamic regulation of extracellular potassium levels, independently of glutamate homeostasis or metabolic support. Using a novel facilitation-depression model, we identified neuronal afterhyperpolarization as the key parameter underlying bursting patterns regulation by extracellular potassium in mice with disconnected astrocytes. We confirmed experimentally this prediction, and revealed that astroglial network-control of extracellular potassium sustains neuronal afterhyperpolarization via activation of KCNQ voltage-gated K+ channels. Altogether, these data delineate how astroglial gap-junctions mechanistically strengthen neuronal population bursts, and points to approaches for controlling aberrant activity in neurological diseases.

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bioRxiv2022

Astrocytes in the retinorecipient superior colliculus display unique cellular and structural properties

Astrocytes have long been considered to be a largely homogeneous cell population. Recent studies however suggest that astrocytes are highly adapted to the local neuronal circuitry. Glucose utilization in the retinorecipient superior colliculus (SC) is one of the highest in the brain. Since metabolic support to neurons is a major function of astrocytes, they could be of particular relevance in this region and display specific features. However, little is known about astrocytes and their interactions with neurons in this multisensory brain area. We thus here investigated region-specific cellular and structural properties of astrocytes in the visual layer of the SC. Using morphological reconstructions, fluorescent recovery after photobleaching (FRAP) and superresolution imaging, we found that astrocytes from the visual layers of the SC are highly distinct with a higher cellular density, a more complex morphology and a stronger proximity to synapses compared to astrocytes from the primary visual cortex and the hippocampus. These data point to astroglial diversity and specialization within neural circuits integrating sensory information in the adult brain.

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bioRxiv2022

Translational regulation by RACK1 in astrocytes represses KIR4.1 expression and regulates neuronal activity

The regulation of translation in astrocytes, the main glial cells in the brain, remains poorly characterized. We developed a high-throughput proteomic screen for polysome-associated proteins in astrocytes and focused on the ribosomal protein receptor of activated protein C kinase 1 (RACK1), a critical factor in translational regulation. In astrocyte somata and perisynaptic astrocytic processes (PAPs), RACK1 preferentially bound to a number of mRNAs, including Kcnj10, encoding the inward rectifying potassium (K+) channel KIR4.1, a critical astrocytic regulator of neurotransmission. By developing an astrocyte-specific, conditional RACK1 knock-out mouse model, we showed that RACK1 repressed the production of KIR4.1 in hippocampal astrocytes and PAPs. Reporter-based assays revealed that RACK1 controlled Kcnj10 translation through the transcripts 5 untranslated region. Upregulation of KIR4.1 in the absence of RACK1 modified the astrocyte territory volume and neuronal activity attenuatin burst frequency and duration in the hippocampus. Hence, astrocytic RACK1 represses KIR4.1 translation and influences neuronal activity.

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bioRxiv2022

Astrocytes regulate locomotion by orchestrating neuronal rhythmicity in the spinal network via potassium clearance

SO_SCPLOWUMMARYC_SCPLOWNeuronal rhythmogenesis in the spinal cord is correlated with variations in extracellular K+ levels ([K+]e). Astrocytes play important role in[K+]e homeostasis and compute neuronal information. Yet it is unclear how neuronal oscillations are regulated by astrocytic K+ homeostasis. Here we identify the astrocytic inward-rectifying K+ channel Kir4.1 (a.k.a. Kcnj10) as a key molecular player for neuronal rhythmicity in the spinal central pattern generator (CPG). By combining two-photon calcium imaging with electrophysiology, immunohistochemistry and genetic tools, we report that astrocytes display Ca2+ transients before and during oscillations of neighbouring neurons. Inhibition of astrocytic Ca2+ transients with BAPTA decreases the barium-sensitive Kir4.1 current responsible of K+ clearance. Finally, we show in mice that Kir4.1 knockdown in astrocytes progressively prevents neuronal oscillations and alters the locomotor pattern resulting in lower motor performances in challenging tasks. These data identify astroglial Kir4.1 channels as key regulators of neuronal rhythmogenesis in the CPG driving locomotion. SO_SCPLOWIGNIFICANCEC_SCPLOWO_SCPCAP C_SCPCAPO_SCPLOWSTATEMENTC_SCPLOWDespite decades of research, the cellular mechanisms responsible of the synchronized rhythmic oscillations driving locomotion remain elusive. To gain insight into the function of the spinal locomotor network, numerous studies have characterized diverse classes of locomotor-related neurons to determine their role in generating rhythmic movements during locomotion. In contrast, studies investigating non-neuronal components of the spinal cord are sparse. Our study represents a significant breakthrough by identifying astrocytic K+ uptake as a key regulator of neuronal rhythmicity synchronization and locomotor pattern at the cellular, microcircuit and system levels. These data provide mechanistic insights into the neuroglial dialogue at play during rhythmogenesis and point to a novel astroglial target for restoring normal neuronal network excitability in brain disorders and neurodegenerative diseases.

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bioRxiv2020

Physiological synaptic activity and recognition memory are fueled by astroglial glutamine

Presynaptic glutamate replenishment is fundamental to brain function. In high activity regimes, such as epileptic episodes, this process is thought to rely on the glutamate-glutamine cycle between neurons and astrocytes. However the presence of an astroglial glutamine supply, as well as its functional relevance in vivo in the healthy brain remain controversial, partly due to a lack of tools that can directly examine glutamine transfer. Here, we generated a novel fluorescent probe that tracks glutamine in live cells, which provided direct visual evidence of an activity-dependent glutamine supply from astroglial networks to presynaptic structures under physiological conditions. This mobilization is mediated by connexin43, an astroglial protein with both gap-junction and hemichannel functions, and is essential for synaptic transmission and object recognition memory. Our findings uncover an indispensable recruitment of astroglial glutamine in physiological synaptic activity and memory via an unconventional pathway, thus providing an astrocyte basis for cognitive processes.

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