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Dive into the research topics where Carole Rovère is active.

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Featured researches published by Carole Rovère.


Neuroscience | 2009

Long term exposure to the chemokine CCL2 activates the nigrostriatal dopamine system: a novel mechanism for the control of dopamine release

Alice Guyon; Delphine Skrzydelski; I. De Giry; Carole Rovère; G. Conductier; J.M. Trocello; Valérie Daugé; Patrick Kitabgi; William Rostène; Jean-Louis Nahon; S. Mélik Parsadaniantz

Accumulating evidence show that chemokines can modulate the activity of neurons through various mechanisms. Recently, we demonstrated that CCR2, the main receptor for the chemokine CCL2, is constitutively expressed in dopamine neurons in the rat substantia nigra. Here we show that unilateral intranigral injections of CCL2 (50 ng) in freely moving rats increase extracellular concentrations of dopamine and its metabolites and decrease dopamine content in the ipsilateral dorsal striatum. Furthermore, these CCL2 injections are responsible for an increase in locomotor activity resulting in contralateral circling behavior. Using patch-clamp recordings of dopaminergic neurons in slices of the rat substantia nigra, we observed that a prolonged exposure (>8 min) to 10 nM CCL2 significantly increases the membrane resistance of dopaminergic neurons by closure of background channels mainly selective to potassium ions. This leads to an enhancement of dopaminergic neuron discharge in pacemaker or burst mode necessary for dopamine release. We provide here the first evidence that application of CCL2 on dopaminergic neurons increases their excitability, dopamine release and related locomotor activity.


Journal of Neurochemistry | 2007

The chemokine stromal cell-derived factor-1/CXCL12 activates the nigrostriatal dopamine system

Delphine Skrzydelski; Alice Guyon; Valérie Daugé; Carole Rovère; Emmanuelle Apartis; Patrick Kitabgi; Jean-Louis Nahon; William Rostène; S. Mélik Parsadaniantz

We recently demonstrated that dopaminergic (DA) neurons of the rat substantia nigra constitutively expressed CXCR4, receptor for the chemokine stromal cell‐derived factor‐1 (SDF‐1)/CXCL12 (SDF‐1). To check the physiological relevance of such anatomical observation, in vitro and in vivo approaches were used. Patch clamp recording of DA neurons in rat substantia nigra slices revealed that SDF‐1 (10u2003nmol/L) induced: (i) a depolarization and increased action potential frequency; and (ii) switched the firing pattern of depolarized DA neurons from a tonic to a burst firing mode. This suggests that SDF‐1 could increase DA release from neurons. Consistent with this hypothesis, unilateral intranigral injection of SDF‐1 (50u2003ng) in freely moving rat decreased DA content and increased extracellular concentrations of DA and metabolites in the ipsilateral dorsal striatum, as shown using microdialysis. Furthermore, intranigral SDF‐1 injection induced a contralateral circling behavior. These effects of SDF‐1 were mediated via CXCR4 as they were abrogated by administration of a selective CXCR4 antagonist. Altogether, these data demonstrate that SDF‐1, via CXCR4, activates nigrostriatal DA transmission. They show that the central functions of chemokines are not restricted, as originally thought, to neuroinflammation, but extend to neuromodulatory actions on well‐defined neuronal circuits in non‐pathological conditions.


Frontiers in Neuroendocrinology | 2011

Chemokines and chemokine receptors: New actors in neuroendocrine regulations

William Rostène; Alice Guyon; Lara Kular; David Godefroy; Federica Barbieri; Adriana Bajetto; Ghazal Banisadr; Céline Callewaere; Grégory Conductier; Carole Rovère; Stéphane Melik-Parsadaniantz; Tullio Florio

Chemokines are small secreted proteins that chemoattract and activate immune and non-immune cells. Their role in the immune system is well-known, and it has recently been suggested that they may also play a role in the central nervous system (CNS). Indeed, they do not only act as immunoinflammatory mediators in the brain but they also act as potential modulators in neurotransmission. Although we are only beginning to be aware of the implication of chemokines in neuroendocrine functions, this review aims at summarizing what is known in that booming field of research. First we describe the expression of chemokines and their receptors in the CNS with a focus on the hypothalamo-pituitary system. Secondly, we present what is known on some chemokines in the regulation of neuroendocrine functions such as cell migration, stress, thermoregulation, drinking and feeding as well as anterior pituitary functions. We suggest that chemokines provide a fine modulatory tuning system of neuroendocrine regulations.


The Journal of Comparative Neurology | 2000

Regional and cellular localization of the neuroendocrine prohormone convertases PC1 and PC2 in the rat central nervous system.

Raphaelle Winsky-Sommerer; Suzanne Benjannet; Carole Rovère; Pierre Barbero; Nabil G. Seidah; Jacques Epelbaum; Pascal Dournaud

PC1 and PC2 are two major enzymes involved in the processing of protein precursors directed to the regulated secretory pathway. Whereas transcripts encoding both enzymes are widely distributed in the central nervous system, information regarding the localization of proteins themselves is still lacking. In an attempt to gain insight into the neurobiologic roles of PC1 and PC2, both enzymes were immunolocalized in the rat brain by using C‐terminally directed antibodies, which respectively recognize the 87‐kDa PC1 and the 75 and 68‐kDa PC2 forms. Adjacent sections immunoreacted with PC1 or PC2 antibodies exhibited selective patterns of immunostaining in regions well characterized with respect to their biosynthesis of multiple neuropeptides such as the cerebral cortex, hippocampus, and hypothalamus. PC1 signal intensity was generally weaker than that of PC2, although both enzymes displayed extensive overlapping patterns of expression. As assessed by double‐labeling experiments at the cellular level, PC1 and PC2 immunoreactive signals were localized within the trans‐Golgi network and nerve terminals, in keeping with the biosynthetic pathways of neuropeptides. Immunoreactive fibers were detected in many areas throughout the brain but were particularly densely distributed in the hypothalamus and the brainstem. Both enzymes were also localized within dendrites of numerous neurons, supporting the hypothesis that dendritic neuropeptide maturation and release may occur in a large number of brain regions. Taken together, our results provide new evidence that both convertases are efficiently targeted to the neuronal regulated secretory pathway and are well poised to process protein precursors in biologically active end‐products within the mammalian brain. J. Comp. Neurol. 424:439–460, 2000.


Peptides | 2009

Melanin-concentrating hormone producing neurons: Activities and modulations

Alice Guyon; Grégory Conductier; Carole Rovère; Antoine Enfissi; Jean-Louis Nahon

Regulation of energy homeostasis in animals involves adaptation of energy intake to its loss, through a perfect regulation of feeding behavior and energy storage/expenditure. Factors from the periphery modulate brain activity in order to adjust food intake as needed. Particularly, first order neurons from arcuate nucleus are able to detect modifications in homeostatic parameters and to transmit information to second order neurons, partly located in the lateral hypothalamic area. These second order neurons have widespread projections throughout the brain and their proper activation leads them to a coordinated response associated to an adapted behavior. Among these neurons, melanin-concentrating hormone (MCH) expressing neurons play an integrative role of the various factors arising from periphery, first order neurons and extra-hypothalamic arousal systems neurons and modulate regulation of feeding, drinking and seeking behaviors. As regulation of MCH release is correlated to regulation of MCH neuronal activity, we focused this review on the electrophysiological properties of MCH neurons from the lateral hypothalamic area. We first reviewed the knowledge on the endogenous electrical properties of MCH neurons identified according to various criteria which are described. Then, we dealt with the modulations of the electrical activity of MCH neurons by different factors such as glucose, glutamate and GABA, peptides and hormones regulating feeding and transmitters of extra-hypothalamic arousal systems. Finally, we described the current knowledge on the modulation of MCH neuronal activity by cytokines and chemokines. Because of such regulation, MCH neurons are some of the best candidate to account for infection-induced anorexia, but also obesity.


European Journal of Neuroscience | 2005

Complex effects of stromal cell-derived factor-1α on melanin-concentrating hormone neuron excitability

Alice Guyon; G. Banisadr; Carole Rovère; A. Cervantes; P. Kitabgi; Stéphane Melik-Parsadaniantz; Jean-Louis Nahon

Stromal cell‐derived factoru20031α (SDF‐1α), a chemoattractant for leucocytes and neurons, and its receptor, CXCR4 are expressed in subsets of neurons of specific brain areas. In rat lateral hypothalamic area (LHA) we show, using immunocytochemistry, that CXCR4 is localized within melanin‐concentrating hormone (MCH)‐expressing neurons, mainly involved in feeding behaviour regulation. We investigated whether SDF‐1α may control MCH neuronal activity. Patch‐clamp recordings in rat LHA slices revealed multiple effects of SDF‐1α on the membrane potential of MCH neurons, indirect through glutamate/GABA release and direct through GIRK current activation. Moreover, SDF‐1α at 0.1–1u2003nm decreased peak and discharge frequency of action potential evoked by current pulses. These effects were further confirmed in voltage‐clamp experiments, SDF‐1α depressing both potassium and sodium currents. At 10u2003nm, however, SDF‐1α increased peak and discharge frequency of action potential evoked by current pulses. Using a specific CXCR4 antagonist, we demonstrated that only the depressing effect on AP discharge was mediated through CXCR4 while the opposite effect was indirect. Together, our studies reveal for the first time a direct effect of SDF‐1α on voltage‐dependent membrane currents of neurons in brain slices and suggest that this chemokine may regulate MCH neuron activity.


Journal of Neuroimmunology | 2008

How cytokines can influence the brain: A role for chemokines?

Alice Guyon; Fabienne Massa; Carole Rovère; Jean-Louis Nahon

Following inflammation or infection, cytokines are released in the blood. Besides their effect on the immune system, cytokines can also act in the brain to modulate our behaviors, inducing for example anorexia when produced in large amount. This review focuses on our current knowledge on how cytokines can influence the brain and the behaviors through several possible pathways: modulating peripheral neurons which project to the brain through the vagus nerve, modulating the levels of hormones such as leptin which can act to the brain through the humoral pathway and possibly acting directly in the brain, through the local production of cytokines and chemokines such as SDF-1alpha/CXCL12.


Journal of Neurochemistry | 2005

Stromal cell-derived factor-1α directly modulates voltage-dependent currents of the action potential in mammalian neuronal cells

Alice Guyon; Carole Rovère; A. Cervantes; I. Allaeys; Jean-Louis Nahon

Stromal cell‐derived factor‐1α (SDF‐1α) is a chemokine whose receptor, CXCR4, is distributed in specific brain areas including hypothalamus. SDF‐1α has recently been found to play important roles in neurons, although direct modulation of voltage‐gated ionic channels has never been shown. In order to clarify this issue, we performed patch‐clamp experiments in fetal mouse hypothalamic neurons in culture. SDF‐1α (10u2003nm) decreased the peak and rising slope of the action potentials and spike discharge frequency in 22% of hypothalamic neurons tested. This effect was blocked by the CXCR4 antagonist AMDu20033100 (1u2003µm) but not by the metabotropic glutamate receptor antagonist MCPG (500u2003µm), indicating a direct action of SDF‐1α on its cognate receptor. This effect involved a depression of both inward and outward voltage‐dependent currents of the action potential. We confirmed these effects in the human neuroblastoma cell line SH‐SY5Y, which endogenously expresses CXCR4. Voltage‐clamp experiments revealed that SDF‐1α induced a 20% decrease in the peak of the tetrodotoxin‐sensitive sodium current and tetraethylammonium‐sensitive delayed rectifier potassium current, respectively. Both effects were concentration dependent, and blocked by AMDu20033100 (200u2003nm). This dual effect was reduced or blocked by 0.4u2003mm GTPγS G‐protein pre‐activation or by pre‐treatment with the G‐protein inhibitor pertussis toxin (200u2003ng/mL), suggesting that it is mediated via activation of a Gi/ou2003protein. This study extends the functions of SDF‐1α to a direct modulation of voltage‐dependent membrane currents of neuronal cells.


Annals of the New York Academy of Sciences | 2015

The complex contribution of chemokines to neuroinflammation: switching from beneficial to detrimental effects

Ophélia Le Thuc; Nicolas Blondeau; Jean-Louis Nahon; Carole Rovère

Inflammation is an innate mechanism that defends organisms against harmful stimuli. Inflammation leads to the production and secretion of proinflammatory mediators that activate and recruit immune cells to damaged tissues, including the brain, to resolve the cause of inflammation. In the central nervous system, inflammation is referred to as neuroinflammation, which occurs in various pathological conditions of the brain. The primary role of neuroinflammation is to protect the brain. However, prolonged and/or inappropriate inflammation can be harmful for the brain, from individual cells to the whole tissue. This review focuses on a particular type of inflammatory mediator, chemokines, and describes their complex effects both under physiological and pathophysiological conditions of the brain. The clinical relevance of the multiple characters of chemokines is highlighted with respect to acute and chronic inflammation of the brain, including their actions in stroke and Alzheimers disease, respectively.


Peptides | 2009

Melanin-concentrating hormone induces neurite outgrowth in human neuroblastoma SH-SY5Y cells through p53 and MAPKinase signaling pathways

Natacha Cotta-Grand; Carole Rovère; Alice Guyon; Alexandra Cervantes; Frédéric Brau; Jean-Louis Nahon

Melanin-concentrating hormone (MCH) peptide plays a major role in energy homeostasis regulation. Little is known about cellular functions engaged by endogenous MCH receptor (MCH-R1). Here, MCH-R1 mRNA and cognate protein were found expressed in human neuroblastoma SH-SY5Y cells. Electrophysiological experiments demonstrated that MCH modulated K(+) currents, an effect depending upon the time of cellular growth. MCH treatments induced a transient phosphorylation of MAPKinases, abolished by PD98059, and partially blocked by PTX, suggesting a Galphai/Galphao protein contribution. MCH stimulated expression and likely nuclear localization of phosphorylated p53 proteins, an effect fully dependent upon MAPKinase activities. MCH treatment also increased phosphorylation of Elk-1 and up-regulated Egr-1, two transcriptional factors targeted by the MAPKinase pathway. Finally, MCH provoked neurite outgrowth after 24h-treatment of neuroblastoma cells. This effect and transcriptional factors activation were partly prevented by PD98059. Collectively, our results provide the first evidence for a role of MCH in neuronal differentiation of endogenously MCH-R1-expressing cells via non-exclusive MAPKinase and p53 signaling pathways.

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Jean-Louis Nahon

Centre national de la recherche scientifique

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Alice Guyon

Centre national de la recherche scientifique

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Nicolas Blondeau

Centre national de la recherche scientifique

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Ophélia Le Thuc

Centre national de la recherche scientifique

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Grégory Conductier

Centre national de la recherche scientifique

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A. Cervantes

Centre national de la recherche scientifique

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Catherine Heurteaux

Centre national de la recherche scientifique

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Céline Cansell

Centre national de la recherche scientifique

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Katharina Stobbe

Centre national de la recherche scientifique

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Patrick Kitabgi

French Institute of Health and Medical Research

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