WorldCat Identities

Roux, Lisa (1984-....).

Overview
Works: 6 works in 7 publications in 2 languages and 8 library holdings
Roles: Opponent, Author
Publication Timeline
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Most widely held works by Lisa Roux
Neuroglial network interactions in the olfactory glomeruli by Lisa Roux( Book )

2 editions published in 2011 in English and held by 3 WorldCat member libraries worldwide

Une des propriétés caractéristiques des astrocytes est leur niveau d'expression élevé en connexines, les protéines constitutives des jonctions communicantes, à la base de leur organisation en réseaux. L'objectif de cette thèse a été de comprendre comment les neurones et les astrocytes interagissent non pas à l'échelle cellulaire, comme cela a généralement été étudié, mais au niveau des réseaux multicellulaires. Cette étude a été menée dans les glomérules olfactifs où les circuits neuronaux forment des unités fonctionnelles bien définies. Des expériences de «dye coupling» réalisées sur des tranche aigues de bulbe olfactif de souris, ont tout d'abord permis d'établir que (1) l'organisation spatiale des réseaux astrocytaires reflète les unités fonctionnelles glomérulaires et (2) qu'ils sont régulés par l'activité neuronale ainsi que l'expérience olfactive. La contribution des réseaux astrocytaires à l'activité de réseau du bulbe olfactif a ensuite été étudiée in vitro. Une activité rythmique (<1Hz), dépendante des interactions neuronales au sein du glomérule, a été observée dans les cellules mitrales. Ses caractéristiques s'apparentent aux oscillations lentes enregistrées pendant le sommeil dans le système thalamo-cortical. Des souris transgéniques dépourvues de connexines astrocytaires ont permis de montrer que les astrocytes modulent cette activité de réseau via ces protéines. Ces résultats mettent en évidence une boucle d'interactions réciproques entre réseaux neuronaux et astrocytaires. Ils suggèrent qu'un tel dialogue pourrait jouer un rôle dans les relations bulbe olfactif - cortex qui, à la différence des autres systèmes sensoriels, sont dépourvues de relais thalamique
Rôles des récepteurs cannabinoïdes de type 1 dans le cortex piriforme antérieur by Geoffrey Terral( )

1 edition published in 2018 in French and held by 1 WorldCat member library worldwide

Being involved in many behavioral functions, olfaction has powerful influence in guiding our actions. Odors communicate with the central nervous system via specialized receptors in the nose olfactory epithelium that generate neuronal signals, which in turn are eventually distributed and processed in many brain regions. In particular, the anterior piriform cortex (aPC) is an important olfactory area involved in perception and integration of odors. Given the extended role of the main cannabinoid type-1 (CB1) receptor in sensory and memory brain functions, we hypothesized that CB1 receptors could modulate odor processing in the aPC. To this aim, using a combination of anatomical, electrophysiological, and pharmacological approaches, we first characterized the distribution of CB1 receptors and their ability to regulate aPC circuits. We found that CB1 receptors are mainly expressed in GABAergic interneurons where their activation regulates inhibitory transmission and plasticity. Then, we evaluated the role and the impact of CB1 receptor modulation on odor-related aPC processing. In vivo calcium imaging revealed that odor-evoked aPC activity is affected by alteration of CB1 receptor signaling. Additionally, we demonstrated that physiological aPC-CB1 receptors functioning is necessary for retrieve appetitive but not aversive olfactory memory, likely through modulation of local inhibitory circuits. Overall, this work contribute to a better understanding of how CB1 receptors modulate olfactory processes in the aPC
Contribution of the potassium / chloride cotransporter KCC2 to hippocampal rhythmopathy by Marie Goutierre( )

1 edition published in 2018 in English and held by 1 WorldCat member library worldwide

Dans le système nerveux central, la transmission inhibitrice est principalement assurée par le relargage du neurotransmetteur GABA dans la fente synaptique. La fixation du GABA sur les récepteurs GABAA induit en effet un flux entrant d'ions chlorure, résultant en une hyperpolarisation du neurone. Le maintien d'une faible concentration intraneuronale en chlore est donc essentielle à l'action inhibitrice du GABA. Dans les neurones matures, cette fonction est principalement réalisée grâce à l'activité du transporteur potassium - chlore KCC2 qui exporte en permanence les ions chlorures. Dans de nombreuses pathologies neurologiques, telles que l'épilepsie, le syndrome de Rett ou encore les douleurs neuropathiques, on observe une diminution de l'expression de KCC2. Cela conduit à une élévation du niveau de chlore intraneuronal et à une altération de la transmission GABAergique. Cet effet est supposé être à la base de nombre des symptômes observés dans les pathologies citées précédemment. Cependant, KCC2 est également fortement exprimé à proximité des synapses glutamatergiques. Sa présence influence ainsi l'efficacité de la transmission excitatrice et est nécessaire à l'expression de la potentialisation à long terme des synapses. Ces fonctions inattendues de KCC2 aux synapses excitatrice ne reposent pas sur sa fonction de transport de chlore mais plutôt sur ses interactions avec diverses protéines. Ainsi, le transporteur KCC2 possède de multiple fonctions et régule différemment les transmissions excitatrice et inhibitrice. Prédire l'effet de la perte du transporteur sur l'activité globale d'un réseau neuronal est donc compliqué. Durant ma thèse, j'ai caractérisé les effets de la suppression de KCC2 dans les cellules en grains du gyrus denté sur leurs propriétés cellulaires, synaptiques et sur l'activité du réseau hippocampique. De façon inattendue, j'ai montré que la perte de KCC2 ne s'accompagnait pas de modifications majeures de la transmission inhibitrice. En revanche, j'ai mis en évidence un nouveau mécanisme indépendant du transport de chlore par lequel KCC2 contrôle l'excitabilité des neurones et la rythmogénèse hippocampique à travers son interaction avec le canal potassique Task-3. Mes résultats prédisent que les déficits associés à une perte de KCC2 pourraient être en partie expliqués par cet effet sur l'excitabilité. Ils suggèrent également que Task-3 pourrait constituer une nouvelle cible thérapeutique dans le traitement de ces pathologies
Tasks for inhibitory interneurons in intact brain circuits( )

1 edition published in 2015 in English and held by 1 WorldCat member library worldwide

Abstract: Synaptic inhibition, brought about by a rich variety of interneuron types, counters excitation, modulates the gain, timing, tuning, bursting properties of principal cell firing, and exerts selective filtering of synaptic excitation. At the network level, it allows for coordinating transient interactions among the principal cells to form cooperative assemblies for efficient transmission of information and routing of excitatory activity across networks, typically in the form of brain oscillations. Recent techniques based on targeted expression of neuronal activity modulators, such as optogenetics, allow physiological identification and perturbation of specific interneuron subtypes in the intact brain. Combined with large-scale recordings or imaging techniques, these approaches facilitate our understanding of the multiple roles of inhibitory interneurons in shaping circuit functions. This article is part of the Special Issue entitled 'GABAergic Signaling in Health and Disease'. Highlights: Inhibition secures transient autonomy of principal cells. Inhibitory interneurons are the backbone of brain oscillations. Optogenetics-assisted tagging of interneuron subtypes improves correlative studies. Cell-type specific manipulations clarify the roles of interneurons in computation
Dynamique des interactions entre excitation et inhibition périsomatique dans le circuit hippocampique normal et épileptique in vivo by Olivier Dubanet( )

1 edition published in 2019 in French and held by 1 WorldCat member library worldwide

The hippocampus is a key structure for learning and memory. The function of this neuronal circuit is based on complex interactions between excitatory glutamatergic pyramidal cells and various types of inhibitory GABAergic interneurons. The precise roles fullfiled by interneuron subtypes is still unclear because it is challenging to study in vivo the inhibitory function of specific interneurons. Alterations of the synaptic interactions between pyramidal cells and interneurons in the hippocampus also underlie neurological pathologies such as epilepsy, neurodevelopmental diseases such as autism, or neurodegenerative diseases such as Alzheimer's disease. Among the different types of interneurons, those that express parvalbumin (PV) and project to pyramidal cell bodies (perisomatic inhibition) are particularly efficient in blocking action potential generation in their target cells. PV interneurons therefore play a central role in neuronal coding (by controlling which cell can fire or not) but also in the balance between global excitation and inhibition within the circuit, prevention runaway excitation between interconnected pyramidal cells and the generation of epileptic seizure. Functional perisomatic inhibition directly depends on Cl- electrochemical gradient, or the interaction between membrane potential and Cl- distribution across the membrane of the target neuron. However, these parameters change continuously during neuronal activity, and it has been shown that the Cl- gradient can be reversed, resulting in paradoxically excitatory GABAergic transmission. This phenomenon, which contributes to the physiological maturation of neuronal circuits during early development, is also considered as a major source of neuronal circuit dysfunction in various pathologies such as epilepsy, autism or schizophrenia. This field of research is therefore clinically relevant, and the research for drugs restoring a physiological Cl- gradient is very active. However, a direct assessment of the excitatory GABA hypothesis has been hindered by the technical difficulty of probing endogenous GABAergic synaptic function in vivo, and contradictory data in the literature call for a direct evaluation. During my PhD, using electrophysiological, opto- and pharmaco-genetic techniques, I have contributed to develop a new and sophisticated methodological approach to evaluate the perisomatic GABAergic transmission in the hippocampus, respecting the complexity of spontaneous neuronal activity dynamics in vivo. I have studied the functional role of perisomatic inhibition from PV interneurons in the adult hippocampal circuit, in physiological conditions and in two models of epileptic mice in which I was able to detect an excitatory GABAergic transmission in vivo. However, excitatory GABA was unlikely to participate in epileptogenesis because it was expressed only during the period of post-ictal silence after acute seizures, or in a potentially negligible minority of pyramidal cells one week post-status epilepticus during the latent period that precedes the emergence of chronic epilepsy, a stage during which I also demonstrated that the majority of CA3 pyramidal neurons were no longer under perisomatic inhibitory control. In addition to contribute to a better understanding of epileptogenesis, this approach constitutes an invaluable tool to quantify the actual in vivo efficacy of drugs designed to modulate Cl- homeostasis and restore physiological GABAergic inhibition, thereby meeting high clinical and therapeutical expectations
Les cellules du tronc cérébral exprimant la somatostatine contrôlent la régulation émotionnelle du comportement de la douleur by Nânci Winke( )

1 edition published in 2021 in French and held by 1 WorldCat member library worldwide

When facing a danger, mammals display a broad range of defensive fear responses among which the most studied are freezing and avoidance. Beside these responses, analgesia has also been reported to be an important defensive response to an aversive or noxious stimulus. Indeed, following fear conditioning, presentation of the conditioned stimulus (CS) lead to a reduction in pain sensitivity, a phenomenon known as fear conditioned analgesia (FCA). FCA is supposed to result from the activation of descending pathways directly modulating pain processing in the dorsal horn (DH) of the spinal cord. A number of studies have identified over the past decades the neurochemistry of FCA and identified the GABAergic, endocannabinoid and opioidergic systems as key components of the analgesic responses observed upon FCA. However, to date the precise circuits and mechanisms involved in this phenomenon are largely unknown. Several brain regions, including the medial prefrontal cortex (mPFC), the central nucleus of the amygdala (CeA) and the ventrolateral periaqueductal gray (vlPAG) have been involved both in fear and pain processing. More specifically the vlPAG, the brain output structure mediating fear behavior receives strong inputs from the CeA and the mPFC and is necessary for freezing responses. Interestingly, the vlPAG is also a key structure in pain modulation as its electrical stimulation induces analgesia and vlPAG neurons respond to nociceptive information. Thus, although it is clearly established that fear and pain processes interact in the vlPAG, the precise organization of vlPAG microcircuits and the mechanisms by which fear modulates pain sensitivity during FCA, remain unknown. Using a combination of behavioral, anatomical, optogenetic and electrophysiological approaches we show that somatostatin-expressing neurons in the ventrolateral periaqueductal gray matter (vlPAG SST cells) promote antinoceptive responses during presentation of conditioned stimuli predicting footstocks. Whereas the optogenetic inhibition of vlPAG SST cells promoted analgesia, their optogenetic activation reduced analgesia by potentiating pain responses in the spinal cord through a relay in the rostral ventromedial medulla (RVM). Together these results identify a brainstem circuit composed of vlPAG SST cells specifically projecting to the RVM and mediating FCA to regulate pain responses during threatful situations
 
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Alternative Names
Lisa Roux wetenschapper

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