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1. Early reduced dopaminergic tone mediated by D3 receptor and dopamine transporter in absence epileptogenesis

Author

Cavarec, Fanny, Krauss, Philipp, Witkowski, Tiffany, Broisat, Alexis, Ghezzi, Catherine, de Gois, Stéphanie, Giros, Bruno, Depaulis, Antoine, and Deransart, Colin

Subjects
Quantitative Biology - Neurons and Cognition
Abstract

Abstract Objective In Genetic Absence Epilepsy Rats From Strasbourg ( GAERS s), epileptogenesis takes place during brain maturation and correlates with increased mRNA expression of D3 dopamine receptors (D3R). Whether these alterations are the consequence of seizure repetition or contribute to the development of epilepsy remains to be clarified. Here, we addressed the involvement of the dopaminergic system in epilepsy onset in GAERS s. Methods Experiments were performed using rats at different stages of brain maturation from three strains according to their increasing propensity to develop absence seizures: nonepileptic control rats ( NEC s), Wistar Hannover rats, and GAERS s. Changes in dopaminergic neurotransmission were investigated using different behavioral and neurochemical approaches: autoradiography of D3R and dopamine transporter, single photon emission computed tomographic imaging, acute and chronic drug effects on seizure recordings (dopaminergic agonists and antagonists), quinpirole-induced yawns and dopamine synaptosomal uptake, microdialysis, brain tissue monoamines, and brain-derived neurotrophic factor quantification. Results Autoradiography revealed an increased expression of D3R in 14-day-old GAERS s, before absence seizure onset, that persists in adulthood, as compared to age-matched NEC s. This was confirmed by increased yawns, a marker of D3R activity, and increased seizures when animals were injected with quinpirole at low doses to activate D3R. We also observed a concomitant increase in the expression and activity of the dopamine transporter in GAERS s before seizure onset, consistent with both lowered dopamine basal level and increased phasic responses. Significance Our data show that the dopaminergic system is persistently altered in GAERS s, which may contribute not only to behavioral comorbidities but also as an etiopathogenic factor in the development of epilepsy. The data suggest that an imbalanced dopaminergic tone may contribute to absence epilepsy development and seizure onset, as its reversion by a chronic treatment with a dopamine stabilizer significantly suppressed epileptogenesis. Our data suggest a potential new target for antiepileptic therapies and/or improvement of quality of life of epileptic patients.

Published
2024
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2. Nucleus accumbens D1- and D2-expressing neurons control the balance between feeding and activity-mediated energy expenditure

Author

Walle, Roman, Petitbon, Anna, Fois, Giulia R., Varin, Christophe, Montalban, Enrica, Hardt, Lola, Contini, Andrea, Angelo, Maria Florencia, Potier, Mylène, Ortole, Rodrigue, Oummadi, Asma, De Smedt-Peyrusse, Véronique, Adan, Roger A., Giros, Bruno, Chaouloff, Francis, Ferreira, Guillaume, de Kerchove d’Exaerde, Alban, Ducrocq, Fabien, Georges, François, and Trifilieff, Pierre

Published
2024
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3. The NeuroD6 subtype of VTA neurons contributes to psychostimulant sensitization and behavioral reinforcement

Author

Bimpisidis, Zisis, König, Niclas, Stagkourakis, Stefanos, Zell, Vivien, Vlcek, Bianca, Dumas, Sylvie, Giros, Bruno, Broberger, Christian, Hnasko, Thomas S, and Wallén-Mackenzie, Åsa

Subjects
Biological Psychology, Pharmacology and Pharmaceutical Sciences, Biomedical and Clinical Sciences, Psychology, Substance Misuse, Mental Health, Basic Behavioral and Social Science, Genetics, Behavioral and Social Science, Drug Abuse (NIDA only), Neurosciences, 2.1 Biological and endogenous factors, Aetiology, Good Health and Well Being, Amphetamine, Animals, Basic Helix-Loop-Helix Transcription Factors, Central Nervous System Stimulants, Cocaine, Corpus Striatum, Dopaminergic Neurons, Ethanol, Female, Locomotion, Male, Mice, Knockout, Nerve Tissue Proteins, Optogenetics, RNA, Messenger, Reward, Ventral Tegmental Area, Vesicular Monoamine Transport Proteins, accumbens, dopamine, mouse genetics, optogenetics, reward, ventral tegmental area
Abstract

Reward-related behavior is complex and its dysfunction correlated with neuropsychiatric illness. Dopamine (DA) neurons of the ventral tegmental area (VTA) have long been associated with different aspects of reward function, but it remains to be disentangled how distinct VTA DA neurons contribute to the full range of behaviors ascribed to the VTA. Here, a recently identified subtype of VTA neurons molecularly defined by NeuroD6 (NEX1M) was addressed. Among all VTA DA neurons, less than 15% were identified as positive for NeuroD6. In addition to dopaminergic markers, sparse NeuroD6 neurons expressed the vesicular glutamate transporter 2 (Vglut2) gene. To achieve manipulation of NeuroD6 VTA neurons, NeuroD6(NEX)-Cre-driven mouse genetics and optogenetics were implemented. First, expression of vesicular monoamine transporter 2 (VMAT2) was ablated to disrupt dopaminergic function in NeuroD6 VTA neurons. Comparing Vmat2lox/lox;NEX-Cre conditional knock-out (cKO) mice with littermate controls, it was evident that baseline locomotion, preference for sugar and ethanol, and place preference upon amphetamine-induced and cocaine-induced conditioning were similar between genotypes. However, locomotion upon repeated psychostimulant administration was significantly elevated above control levels in cKO mice. Second, optogenetic activation of NEX-Cre VTA neurons was shown to induce DA release and glutamatergic postsynaptic currents within the nucleus accumbens. Third, optogenetic stimulation of NEX-Cre VTA neurons in vivo induced significant place preference behavior, while stimulation of VTA neurons defined by Calretinin failed to cause a similar response. The results show that NeuroD6 VTA neurons exert distinct regulation over specific aspects of reward-related behavior, findings that contribute to the current understanding of VTA neurocircuitry.

Published
2019

4. Nucleus accumbens D1- and D2-expressing neurons control the balance between feeding and activity-mediated energy expenditure

Author

TN groep Adan, Brain, Walle, Roman, Petitbon, Anna, Fois, Giulia R., Varin, Christophe, Montalban, Enrica, Hardt, Lola, Contini, Andrea, Angelo, Maria Florencia, Potier, Mylène, Ortole, Rodrigue, Oummadi, Asma, De Smedt-Peyrusse, Véronique, Adan, Roger A., Giros, Bruno, Chaouloff, Francis, Ferreira, Guillaume, de Kerchove d’Exaerde, Alban, Ducrocq, Fabien, Georges, François, Trifilieff, Pierre, TN groep Adan, Brain, Walle, Roman, Petitbon, Anna, Fois, Giulia R., Varin, Christophe, Montalban, Enrica, Hardt, Lola, Contini, Andrea, Angelo, Maria Florencia, Potier, Mylène, Ortole, Rodrigue, Oummadi, Asma, De Smedt-Peyrusse, Véronique, Adan, Roger A., Giros, Bruno, Chaouloff, Francis, Ferreira, Guillaume, de Kerchove d’Exaerde, Alban, Ducrocq, Fabien, Georges, François, and Trifilieff, Pierre

Published
2024

5. GPR56/ADGRG1 is associated with response to antidepressant treatment

Author

Belzeaux, Raoul, Gorgievski, Victor, Fiori, Laura M., Lopez, Juan Pablo, Grenier, Julien, Lin, Rixing, Nagy, Corina, Ibrahim, El Chérif, Gascon, Eduardo, Courtet, Philippe, Richard-Devantoy, Stéphane, Berlim, Marcelo, Chachamovich, Eduardo, Théroux, Jean-François, Dumas, Sylvie, Giros, Bruno, Rotzinger, Susan, Soares, Claudio N., Foster, Jane A., Mechawar, Naguib, Tall, Gregory G., Tzavara, Eleni T., Kennedy, Sidney H., and Turecki, Gustavo

Published
2020
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9. Antidepressive effects of targeting ELK-1 signal transduction

Author

Apazoglou, Kallia, Farley, Séverine, Gorgievski, Victor, Belzeaux, Raoul, Lopez, Juan Pablo, Grenier, Julien, Ibrahim, El Chérif, El Khoury, Marie-Anne, Tse, Yiu C., Mongredien, Raphaele, Barbé, Alexandre, de Macedo, Carlos E. A., Jaworski, Wojciech, Bochereau, Ariane, Orrico, Alejandro, Isingrini, Elsa, Guinaudie, Chloé, Mikasova, Lenka, Louis, Franck, Gautron, Sophie, Groc, Laurent, Massaad, Charbel, Yildirim, Ferah, Vialou, Vincent, Dumas, Sylvie, Marti, Fabio, Mechawar, Naguib, Morice, Elise, Wong, Tak P., Caboche, Jocelyne, Turecki, Gustavo, Giros, Bruno, and Tzavara, Eleni T.

Published
2018
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13. Dopamine activation of the arachidonic acid cascade as a basis for D1D2 receptor synergism

Author

Piomelli, Daniele, Pilon, Catherine, Giros, Bruno, Sokolofff, Pierre, Martres, Marie-Pascale, and Schwartz, Jean-Charles

Subjects
Neurosciences, 2, 3, 4, 5-Tetrahydro-7, 8-dihydroxy-1-phenyl-1H-3-benzazepine, Adenosine Triphosphate, Animals, Arachidonic Acid, Arachidonic Acids, Calcimycin, Calcium, Cell Line, Cloning, Molecular, Cricetinae, Cricetulus, Drug Synergism, Ergolines, Female, In Vitro Techniques, Ovary, Quinpirole, Rats, Receptors, Dopamine, Signal Transduction, Transfection, General Science & Technology
Abstract

Understanding the actions of the neurotransmitter dopamine in the brain is important in view of its roles in neuropsychiatric illnesses. Dopamine D1 receptors, which stimulate both adenylyl cyclase and phospholipase C, and D2 receptors, which inhibit them, can nevertheless act synergistically to produce many electrophysiological and behavioral responses. Because this functional synergism can occur at the level of single neurons, another, as yet unidentified, signalling pathway activated by dopamine has been hypothesized. We report here that in Chinese hamster ovary (CHO) cells transfected with the D2 receptor complementary DNA, D2 agonists potently enhanced arachidonic acid release, provided that such release has been initiated by stimulating constitutive purinergic receptors or by increasing intracellular Ca2+. In CHO cells expressed D1 receptors, D1 agonists exert no such effect. When D1 and D2 receptors are coexpressed, however, activation of both subtypes results in a marked synergistic potentiation of arachidonic acid release. The numerous actions of arachidonic acid and its metabolites in neuronal signal transduction suggest that facilitation of its release may be implicated in dopaminergic responses, such as feedback inhibition mediated by D2 autoreceptors, and may constitute a molecular basis for D1/D2 receptor synergism.

Published
1991

14. Behavioral and Transcriptomic Changes Following Brain-Specific Loss of Noradrenergic Transmission

Author

Isingrini, Elsa, primary, Guinaudie, Chloé, additional, Perret, Léa, additional, Guma, Elisa, additional, Gorgievski, Victor, additional, Blum, Ian D., additional, Colby-Milley, Jessica, additional, Bairachnaya, Maryia, additional, Mella, Sébastien, additional, Adamantidis, Antoine, additional, Storch, Kai-Florian, additional, and Giros, Bruno, additional

Published
2023
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15. Selective genetic disruption of dopaminergic, serotonergic and noradrenergic neurotransmission: insights into motor, emotional and addictive behaviour

Author

Isingrini, Elsa, Perret, Lea, Rainer, Quentin, Sagueby, Sara, Moquin, Luc, Gratton, Alain, and Giros, Bruno

Subjects
Observations, Genetic aspects, Synaptic transmission -- Observations, Addiction -- Genetic aspects, Emotions -- Genetic aspects, Motor skills -- Genetic aspects, Gene expression -- Observations, Motor ability -- Genetic aspects, Neural transmission -- Observations
Abstract

Introduction Monoaminergic neurotransmitters, namely dopamine (DA), noradrenaline (NE) and serotonin (5-HT), extensively modulate cognitive, affective, neuroendocrine and motor functions in the brain. (1) The role of the monoaminergic systems in [...], Background: The monoaminergic transmitters dopamine (DA), noradrenaline (NE) and serotonin (5-HT) modulate cerebral functions via their extensive effects in the brain. Investigating their roles has led to the creation of vesicular monoaminergic transporter-2 (VMAT2) knockout (KO) mice. While this mutation results in postnatal death, VMAT2- heterozygous (HET) mice are viable and show a complex behavioural phenotype. However, the simultaneous alteration of the 3 systems prevents investigations into their individual functions. Methods: To assess the specific role of NE, 5-HT and DA, we genetically disrupted their neurotransmission by creating conditional VMAT2-KO mice with targeted recombination. These specific recombinations were obtained by breeding [VMAT2.sup.lox/lox] mice with DBHcre, SERTcre and DATcre mice, respectively. We conducted a complete neurochemical and behavioural characterization of VMAT2-HET animals in each system. Results: Conditional VMAT2-KO mice revealed an absence of VMAT2 expression, and a specific decrease in the whole brain levels of each monoamine. Although NE- and 5-HT-depleted mice are viable into adulthood, DA depletion results in postnatal death before weaning. Interestingly, alteration of the DA transmission fully accounted for the increased amphetamine response formerly observed in the VMAT2-HET mice, whereas alteration of the 5-HT system was solely responsible for the increase in cocaine response. Limitations: We used VMAT2-HET mice that displayed a mild phenotype. Because the VMAT2-KO in DA neurons is lethal, it precluded a straightforward comparison of the full KOs in the 3 systems. Conclusion: Given the intermingled functions of NE, 5-HT and DA in regulating cognitive and affective functions, this model will enhance understanding of their respective roles in the pathophysiology of psychiatric disorders.

Published
2016
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19. Impairment of SLC17A8 Encoding Vesicular Glutamate Transporter-3, VGLUT3, Underlies Nonsyndromic Deafness DFNA25 and Inner Hair Cell Dysfunction in Null Mice

Author

Ruel, Jérôme, Emery, Sarah, Nouvian, Régis, Bersot, Tiphaine, Amilhon, Bénédicte, Van Rybroek, Jana M., Rebillard, Guy, Lenoir, Marc, Eybalin, Michel, Delprat, Benjamin, Sivakumaran, Theru A., Giros, Bruno, El Mestikawy, Salah, Moser, Tobias, Smith, Richard J.H., Lesperance, Marci M., and Puel, Jean-Luc

Published
2008
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23. Structural and Functional Characterization of the Interaction of Snapin with the Dopamine Transporter: Differential Modulation of Psychostimulant Actions

Author

Boussicault, Lydie, Kacher, Radhia, Lamaziere, Antonin, Caboche, Jocelyne, Betuing, Sandrine, Potier, Marie-Claude, Erdozain, Amaia, de Gois, Stephanie, Bernard, Véronique, Gorgievski, Victor, Pietrancosta, Nicolas, Dumas, Sylvie, Macedo, Carlos, Vanhoutte, Peter, Ortega, Jorge, Meana, J Javier, Tzavara, Eleni, Vialou, Vincent, Giros, Bruno, Department of Pharmacology [Bizkaia, Spain], University of the Basque Country [Bizkaia] (UPV/EHU), Physiopathologie des maladies psychiatriques = Pathophysiology of Psychiatric Disorders (NPS-07), Neurosciences Paris Seine (NPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut de Biologie Paris Seine (IBPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut de Biologie Paris Seine (IBPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS), Laboratoire de Chimie et de Biochimie Pharmacologiques et Toxicologiques (LCBPT - UMR 8601), Université Paris Descartes - Paris 5 (UPD5)-Centre National de la Recherche Scientifique (CNRS), Laboratoire des biomolécules (LBM UMR 7203), Institut National de la Santé et de la Recherche Médicale (INSERM)-Chimie Moléculaire de Paris Centre (FR 2769), École normale supérieure - Paris (ENS Paris), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Ecole Nationale Supérieure de Chimie de Paris - Chimie ParisTech-PSL (ENSCP), Université Paris sciences et lettres (PSL)-Ecole Superieure de Physique et de Chimie Industrielles de la Ville de Paris (ESPCI Paris), Université Paris sciences et lettres (PSL)-Centre National de la Recherche Scientifique (CNRS)-École normale supérieure - Paris (ENS Paris), Université Paris sciences et lettres (PSL)-Centre National de la Recherche Scientifique (CNRS)-Département de Chimie - ENS Paris, Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Mécanismes adaptatifs : des organismes aux communautés (MAOAC), Muséum national d'Histoire naturelle (MNHN)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC), Neurobiologie des processus adaptatifs (NPA), Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS), Neurobiologie et Psychiatrie, Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM), McGill University = Université McGill [Montréal, Canada], Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université Pierre et Marie Curie - Paris 6 (UPMC), Neurogénétique moléculaire, Université d'Évry-Val-d'Essonne (UEVE)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre de Recherche de l'Institut du Cerveau et de la Moelle épinière (CRICM), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), University of the Basque Country/Euskal Herriko Unibertsitatea (UPV/EHU), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Systèmes glutamatergiques normaux et pathologiques = Normal and Pathologic Glutamatergic Neurons (NPS-05), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Université Paris Descartes - Paris 5 (UPD5)-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS), Analyse, Interactions Moléculaires et Cellulaires (LBM-E2), Chimie Moléculaire de Paris Centre (FR 2769), École normale supérieure - Paris (ENS-PSL), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Ecole Nationale Supérieure de Chimie de Paris - Chimie ParisTech-PSL (ENSCP), Université Paris sciences et lettres (PSL)-Institut de Chimie du CNRS (INC)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-École normale supérieure - Paris (ENS-PSL), Université Paris sciences et lettres (PSL)-Institut de Chimie du CNRS (INC)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Département de Chimie - ENS Paris, Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Chimie Moléculaire de Paris Centre (FR 2769), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Génétique moléculaire de la neurotransmission et des processus neurodégénératifs (LGMNPN), Neuroscience Paris Seine (NPS), Centre National de la Recherche Scientifique (CNRS)-Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC), Université Pierre et Marie Curie - Paris 6 (UPMC)-ESPCI ParisTech-Ecole Nationale Supérieure de Chimie de Paris- Chimie ParisTech-PSL (ENSCP)-Centre National de la Recherche Scientifique (CNRS)-École normale supérieure - Paris (ENS Paris)-Université Pierre et Marie Curie - Paris 6 (UPMC)-ESPCI ParisTech-Ecole Nationale Supérieure de Chimie de Paris- Chimie ParisTech-PSL (ENSCP)-Centre National de la Recherche Scientifique (CNRS)-École normale supérieure - Paris (ENS Paris)-Département de Chimie - ENS Paris, École normale supérieure - Paris (ENS Paris)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Muséum national d'Histoire naturelle (MNHN)-Collège de France (CdF)-Centre National de la Recherche Scientifique (CNRS), Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC), McGill University, Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Centre National de la Recherche Scientifique (CNRS)-Université Paris Descartes - Paris 5 (UPD5), Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS), Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), UPV/EHU Université du Pays Basque, Centro de Investigación Biomédica en Red Salud Mental [Madrid] (CIBER-SAM), Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS)-Université de Paris (UP), Oramacell [Paris, France], École normale supérieure - Paris (ENS Paris)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Ecole Nationale Supérieure de Chimie de Paris- Chimie ParisTech-PSL (ENSCP)-ESPCI ParisTech-Centre National de la Recherche Scientifique (CNRS)-École normale supérieure - Paris (ENS Paris)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Ecole Nationale Supérieure de Chimie de Paris- Chimie ParisTech-PSL (ENSCP)-ESPCI ParisTech-Centre National de la Recherche Scientifique (CNRS)-Département de Chimie - ENS Paris, Vanhoutte, Peter, Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité), and Systèmes glutamatergiques normaux et pathologiques = Normal and Pathologic Glutamatergic Neurons (NPS)

Subjects
Models, Molecular, 0301 basic medicine, Synaptic cleft, Dopamine Plasma Membrane Transport Proteins, Vesicular Transport Proteins, Down-Regulation, Motor Activity, Neurotransmission, Reuptake, Mice, 03 medical and health sciences, 0302 clinical medicine, Dopamine, parasitic diseases, mental disorders, medicine, Animals, [SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], Amphetamine, Cells, Cultured, ComputingMilieux_MISCELLANEOUS, Dopamine transporter, Pharmacology, Binding Sites, biology, Dopaminergic Neurons, Dopaminergic, Brain, Rats, 3. Good health, Psychiatry and Mental health, [SDV.MP]Life Sciences [q-bio]/Microbiology and Parasitology, 030104 developmental biology, nervous system, biology.protein, Original Article, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], Neuroscience, [CHIM.CHEM]Chemical Sciences/Cheminformatics, 030217 neurology & neurosurgery, Protein Binding, medicine.drug
Abstract

International audience; The importance of dopamine (DA) neurotransmission is emphasized by its direct implication in several neurological and psychiatric disorders. The DA transporter (DAT), target of psychostimulant drugs, is the key protein that regulates spatial and temporal activity of DA in the synaptic cleft via the rapid reuptake of DA into the presynaptic terminal. There is strong evidence suggesting that DAT-interacting proteins may have a role in its function and regulation. Performing a two-hybrid screening, we identified snapin, a SNARE-associated protein implicated in synaptic transmission, as a new binding partner of the carboxyl terminal of DAT. Our data show that snapin is a direct partner and regulator of DAT. First, we determined the domains required for this interaction in both proteins and characterized the DAT-snapin interface by generating a 3D model. Using different approaches, we demonstrated that (i) snapin is expressed in vivo in dopaminergic neurons along with DAT; (ii) both proteins colocalize in cultured cells and brain and, (iii) DAT and snapin are present in the same protein complex. Moreover, by functional studies we showed that snapin produces a significant decrease in DAT uptake activity. Finally, snapin downregulation in mice produces an increase in DAT levels and transport activity, hence increasing DA concentration and locomotor response to amphetamine. In conclusion, snapin/DAT interaction represents a direct link between exocytotic and reuptake mechanisms and is a potential target for DA transmission modulation.

Published
2017
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24. Regulation of GluA1 phosphorylation by d-amphetamine and methylphenidate in the cerebellum

Author

Cutando, Laura, Puighermanal, Emma, Castell, Laia, Tarot, Pauline, Bertaso, Federica, Bonnavion, Patricia, de Kerchove d'Exaerde, Alban, Isingrini, Elsa, Galante, Micaela, Dallerac, Glenn, Pascoli, Vincent, Lüscher, Christian, Giros, Bruno B.G., Valjent, Emmanuel, Cutando, Laura, Puighermanal, Emma, Castell, Laia, Tarot, Pauline, Bertaso, Federica, Bonnavion, Patricia, de Kerchove d'Exaerde, Alban, Isingrini, Elsa, Galante, Micaela, Dallerac, Glenn, Pascoli, Vincent, Lüscher, Christian, Giros, Bruno B.G., and Valjent, Emmanuel

Abstract

Prescription stimulants, such as d-amphetamine or methylphenidate are used to treat suffering from attention-deficit hyperactivity disorder (ADHD). They potently release dopamine (DA) and norepinephrine (NE) and cause phosphorylation of the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor subunit GluA1 in the striatum. Whether other brain regions are also affected remains elusive. Here, we demonstrate that d-amphetamine and methylphenidate increase phosphorylation at Ser845 (pS845-GluA1) in the membrane fraction of mouse cerebellum homogenate. We identify Bergmann glial cells as the source of pS845-GluA1 and demonstrate a requirement for intact NE release. Consequently, d-amphetamine-induced pS845-GluA1 was prevented by β1-adenoreceptor antagonist, whereas the blockade of DA D1 receptor had no effect. Together, these results indicate that NE regulates GluA1 phosphorylation in Bergmann glial cells in response to prescription stimulants., SCOPUS: ar.j, info:eu-repo/semantics/published

Published
2020

25. Essential role of beta-adrenergic receptor kinase 1 in cardiac development and function

Author

Jaber, Mohamed, Koch, Walter J., Rockman, Howard, Smith, Bradley, Bond, Richard A., Sulik, Kathleen K., Ross, John, Jr., Lefkowitz, Robert J., Caron, Marc G., and Giros, Bruno

Subjects
Beta adrenoceptors -- Research, Cloning -- Research, Phosphorylation -- Research, Science and technology
Abstract

The [Beta]-adrenergic receptor kinase 1 ([Beta]ARK1) is a member of the G protein-coupled receptor kinase (GRK) family that mediates the agonist-dependent phosphorylation and desensitization of G protein-coupled receptors. We have cloned and disrupted the [Beta]ARK1 gene in mice by homologous recombination. No homozygote [Beta]ARK[1.sup.-/-] embryos survive beyond gestational day 15.5. Prior to gestational day 15.5, [Beta]ARK[1.sup.-/-] embryos display pronounced hypoplasia of the ventricular myocardium essentially identical to the 'thin myocardium syndrome' observed upon gene inactivation of several transcription factors (RXR[Alpha], N-myc, TEF-1, WT-1). Lethality in [Beta]ARK[1.sup.-/-] embryos is likely due to heart failure as they exhibit a [greater than]70% decrease in cardiac ejection fraction determined by direct in utero intra. vital microscopy. These results along with the virtual absence of endogenous GRK activity in [Beta]ARK[1.sup.-/-] embryos demonstrate that [Beta]ARK1 appears to be the predominant GRK in early embryogenesis and that it plays a fundamental role in cardiac development.

Published
1996

26. Hyperlocomotion and indifference to cocaine and amphetamine in mice lacking the dopamine transporter

Author

Giros, Bruno, Jaber, Mohamed, Jones, Sara R., Wightman, R. Mark, and Caron, Marc G.

Subjects
Biological transport -- Research, Carrier proteins -- Physiological aspects, Dopamine -- Physiological aspects, Mice as laboratory animals -- Observations, Cocaine -- Observations, Amphetamines -- Observations, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Homozygote mice devoid of the dopamine transporter (DAT) protein show spontaneous hyperlocomotion, and are unaffected by treatment with the psychostimulants cocaine and amphetamine. DAT is the main factor controlling the neurotransmission of dopamine (DA) and is acted upon by psychostimulants. In its absence, DA persists in the extracellular spaces for a long time although there is a decrease in the amount of D1 and D2 receptors, which are involved in dopamine (DA) responsiveness and enzymes controling DA synthesis. DA controls motor activity, cognition and affect.

Published
1996

28. Identification, characterization, and localization of the dopamine D3 receptor in rat brain using 7-(3H)hydroxy-N,N-di-n-propyl-2-aminotetralin

Author

Levesque, Danie, Diaz, Jorge, Pilon, Catherine, Martres, Marie-Pascale, Giros, Bruno, Souil, Evelyne, Schott, Dominique, Morgat, Jean-Louis, Schwartz, Jean-Charles, and Sokoloff, Pierre

Subjects
Dopamine receptors -- Research, Cells -- Analysis, Neural transmission -- Analysis, Science and technology
Abstract

The existence of the dopamine D3 receptor has been calculated, and its distribution and characteristics in the brain were determined by identifying 7-(H)hydroxy-N,N-di-n-propyl-2-aminotetralin ((H)7-OH-DPAT) as a selective probe for this receptor. (H)7-OH-DPAT binds to D3 receptors with subnanomolar affinity in transfected Chinese hamster ovary cells. A unique pattern of neurotransmission in a confined subpopulation of dopamine neurons probably includes D3 receptors.

Published
1992

30. Antidepressant efficacy of a selective organic cation transporter blocker in a mouse model of depression

Author

Orrico-Sanchez, Alejandro, primary, Chausset-Boissarie, Laetitia, additional, Alves de Sousa, Rodolphe, additional, Coutens, Basile, additional, Rezai Amin, Sara, additional, Vialou, Vincent, additional, Louis, Franck, additional, Hessani, Assia, additional, Dansette, Patrick M., additional, Zornoza, Teodoro, additional, Gruszczynski, Carole, additional, Giros, Bruno, additional, Guiard, Bruno P., additional, Acher, Francine, additional, Pietrancosta, Nicolas, additional, and Gautron, Sophie, additional

Published
2019
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32. Increased vulnerability of nigral dopamine neurons after expansion of their axonal arborization size through D2 dopamine receptor conditional knockout

Author

Giguère, Nicolas, primary, Delignat-Lavaud, Benoît, additional, Herborg, Freja, additional, Voisin, Aurore, additional, Li, Yuan, additional, Jacquemet, Vincent, additional, Anand-Srivastava, Madhu, additional, Gether, Ulrik, additional, Giros, Bruno, additional, and Trudeau, Louis-Éric, additional

Published
2019
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34. Association between the PPP3CC gene, coding for the calcineurin gamma catalytic subunit, and bipolar disorder

Author

Bellivier Frank, Chevalier Fabien, El Khoury Marie-Anne, Etain Bruno, Miot Stéphanie, Mathieu Flavie, Leboyer Marion, Giros Bruno, and Tzavara Eleni T

Subjects
Neurology. Diseases of the nervous system, RC346-429
Abstract

Abstract Background Calcineurin is a neuron-enriched phosphatase that regulates synaptic plasticity and neuronal adaptation. Activation of calcineurin, overall, antagonizes the effects of the cyclic AMP activated protein/kinase A. Thus, kinase/phosphatase dynamic balance seems to be critical for transition to long-term cellular responses in neurons, and disruption of this equilibrium should induce behavioral impairments in animal models. Genetic animal models, as well as post-mortem studies in humans have implicated calcineurin dependent calcium and cyclic AMP regulated phosphorylation/dephosphorylation in both affective responses and psychosis. Recently, genetic association between schizophrenia and genetic variation of the human calcineurin A gamma subunit gene (PPP3CC) has been reported. Methods Based on the assumption of the common underlying genetic factor in schizophrenia and bipolar affective disorder (BPAD), we performed association analysis of CC33 and CCS3 polymorphisms of the PPP3CC gene reported to be associated with schizophrenia in a French sample of 115 BPAD patients and 97 healthy controls. Results Carrying 'CT' or 'TT' genotypes of the PPP3CC-CC33 polymorphism increased risk to develop BPAD comparing to carry 'CC' genotype (OR = 1.8 [1.01–3.0]; p = 0.05). For the PPP3CC-CCS3 polymorphism, 'AG' or 'GG' carriers have an increased risk to develop BPAD than 'AA' carriers (OR = 2.8 [1.5–5.2]). The CC33 and CCS3 polymorphisms were observed in significant linkage disequilibrium (D' = 0.91, r2 = 0.72). Haplotype frequencies were significantly different in BPAD patients than in controls (p = 0.03), with a significant over-transmission of the 'TG' haplotype in BPAD patients (p = 0.001). Conclusion: We suggest that the PPP3CC gene might be a susceptibility gene for BPAD, in accordance with current neurobiological hypotheses that implicate dysregulation of signal-transduction pathways, such as those regulated by calcineurin, in the etiology of affective disorders.

Published
2008
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35. The high efficacy of muscarinic M4 receptor in D1 medium spiny neurons reverses striatal hyperdopaminergia

Author

Nair, Anu G., Castro, Liliana R. V., El Khoury, Marianne, Gorgievski, Victor, Giros, Bruno, Tzavara, Eleni T., Hellgren Kotaleski, Jeanette, Vincent, Pierre, Nair, Anu G., Castro, Liliana R. V., El Khoury, Marianne, Gorgievski, Victor, Giros, Bruno, Tzavara, Eleni T., Hellgren Kotaleski, Jeanette, and Vincent, Pierre

Abstract

The opposing action of dopamine and acetylcholine has long been known to play an important role in basal ganglia physiology. However, the quantitative analysis of dopamine and acetylcholine signal interaction has been difficult to perform in the native context because the striatum comprises mainly two subtypes of medium-sized spiny neurons (MSNs) on which these neuromodulators exert different actions. We used biosensor imaging in live brain slices of dorsomedial striatum to monitor changes in intracellular cAMP at the level of individual MSNs. We observed that the muscarinic agonist oxotremorine decreases cAMP selectively in the MSN sub population that also expresses D-1 dopamine receptors, an action mediated by the M-4 muscarinic receptor. This receptor has a high efficacy on cAMP signaling and can shut down the positive cAMP response induced by dopamine, at acetylcholine concentrations which are consistent with physiological levels. This supports our prediction based on theoretical modeling that acetylcholine could exert a tonic inhibition on striatal cAMP signaling, thus supporting the possibility that a pause in acetylcholine release is required for phasic dopamine to transduce a cAMP signal in D1 MSNs. In vivo experiments with acetylcholinesterase inhibitors donepezil and tacrine, as well as with the positive allosteric modulators of M-4 receptor VU0152100 and VU0010010 show that this effect is sufficient to reverse the increased locomotor activity of DAT-knockout mice. This suggests that M-4 receptors could be a novel therapeutic target to treat hyperactivity disorders., QC 20190328

Published
2019
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36. Increased vulnerability of nigral dopamine neurons after expansion of their axonal arborization size through D2 dopamine receptor conditional knockout

Author

Giguère, Nicolas, Delignat-Lavaud, Benoit, Herborg, Freja, Voisin, Aurore, Li, Yuan, Jacquemet, Vincent, Anand-Srivastava, Madhu, Gether, Ulrik, Giros, Bruno, Trudeau, Louis-Eric, Giguère, Nicolas, Delignat-Lavaud, Benoit, Herborg, Freja, Voisin, Aurore, Li, Yuan, Jacquemet, Vincent, Anand-Srivastava, Madhu, Gether, Ulrik, Giros, Bruno, and Trudeau, Louis-Eric

Published
2019

37. Identification of the neural circuits involved in Attention Deficit Hyperactivity Disorder

Author

Schiffmann, Serge N., de Kerchove d'Exaerde, Alban, Langer, Ingrid, Gall, David, Delvenne, Véronique, Leroy, Karelle, Vanhollebeke, Benoît, Haesler, Sebastian S.H., Giros, Bruno B.G., Pozuelo Fernandez, Elisa, Schiffmann, Serge N., de Kerchove d'Exaerde, Alban, Langer, Ingrid, Gall, David, Delvenne, Véronique, Leroy, Karelle, Vanhollebeke, Benoît, Haesler, Sebastian S.H., Giros, Bruno B.G., and Pozuelo Fernandez, Elisa

Abstract

Attention Deficit Hyperactivity Disorder (ADHD) is a neurodevelopmental psychiatric disorder affecting 5-7% of children and ≈2.5% of adults worldwide, characterized by inattention, by a combination of hyperactivity and impulsivity, or by the three components. Individuals diagnosed with ADHD have an increased risk of educational and occupational failure, accidents, criminality, social disability and developing other psychiatric disorders, being an important burden for the patient and for society.Despite years of research, the etiology of ADHD remains unknown. However, neuroimaging studies demonstrated that ADHD patients display consistent abnormalities in the striatum, the main input nucleus of the basal ganglia, while the precise implication is poorly characterized. The most common pharmacological treatment in ADHD relies on psychostimulants such as amphetamine (Adderall) and methylphenidate (Ritalin). Importantly, in healthy individuals, these drugs stimulate behavioral arousal by increasing the brain efflux of monoamines, while they paradoxically serve to attenuate hyperactivity/impulsivity and improve focus and cognitive performances in ADHD patients. The goals of this thesis are to investigate the implication of one striatal neuronal population in ADHD symptomatology in a transgenic mouse line and to dissect the implication of each monoaminergic system in the paradoxical effects of psychostimulants. First, we developed a new valid mouse model of ADHD characterized by hyperactivity, inattention and motor impulsivity, that displays an ablation of the indirect pathway spiny projection neurons (iSPNs) of the striatum. In addition, in these mice, amphetamine induces a paradoxical reduction of locomotion, which mirrors the calming effect of amphetamine in ADHD patients. In this work, we thus show for the first time the implication of iSPN in attention and impulsivity and suggest a possible role of these neurons in ADHD symptomatology. Further, by using a chemogenetic, Doctorat en Sciences biomédicales et pharmaceutiques (Médecine), info:eu-repo/semantics/nonPublished

Published
2019

40. Cocaine increases dopaminergic connectivity in the nucleus accumbens

Author

Andrianarivelo, Andry, Saint-Jour, Estefani, Trifilieff, Pierre, Cahill, Emma, Bo, Gregory Dal, Dos Santos, Marc, Salery, Marine, Forget, Benoit, Garcia Perez, Maria Alexandra, Betuing, Sandrine, Boudier, Thomas, Sakae, D, Marti, F., Lecca, S, Vorspan, F., Martín-García, E, Morel, L., Henrion, A, Gutierrez-Cuesta, J., Besnard, A., Heck, Nicolas, Herzog, E., Bolte, S., Prado, V, Prado, M., Bellivier, F., Eap, C, Crettol, S, Vanhoutte, Peter, Caboche, Jocelyne, Gratton, A, Moquin, L, Giros, Bruno, Maldonado, R, Daumas, S, Mameli, M., Jamain, S., El Mestikawy, S, Sorbonne Université (SU), Neurosciences Paris Seine (NPS), Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut de Biologie Paris Seine (IBPS), Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS), Institut de Biologie Paris Seine (IBPS), Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), University of Cambridge [UK] (CAM), McGill University = Université McGill [Montréal, Canada], Institut de Recherche Biomédicale des Armées (IRBA), Neuroscience Paris Seine (NPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Nutrition et Neurobiologie intégrée (NutriNeur0), Université Bordeaux Segalen - Bordeaux 2-Institut National de la Recherche Agronomique (INRA)-Université Sciences et Technologies - Bordeaux 1-Institut Polytechnique de Bordeaux-Ecole nationale supérieure de chimie, biologie et physique, Physiopathologie des Maladies du Système Nerveux Central, Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Neuropsychopharmacologie, Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM), Signalisation Neuronale et Régulations Géniques = Neuronal Signaling and Gene Regulation (NPS-02), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Neurogénétique moléculaire, Université d'Évry-Val-d'Essonne (UEVE)-Institut National de la Santé et de la Recherche Médicale (INSERM), Image & Pervasive Access Lab (IPAL), Institute for Infocomm Research - I²R [Singapore]-Centre National de la Recherche Scientifique (CNRS)-Agency for science, technology and research [Singapore] (A*STAR)-MATHEMATIQUES, SCIENCES ET TECHNOLOGIES DE L'INFORMATION ET DE LA COMMUNICATION (UJF)-National University of Singapore (NUS)-Université Pierre et Marie Curie - Paris 6 (UPMC), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Neuropsychopharmacologie des addictions. Vulnérabilité et variabilité expérimentale et clinique (NAVVEC - UM 81 (UMR 8206/ U705)), Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Descartes - Paris 5 (UPD5)-Institut des sciences du Médicament -Toxicologie - Chimie - Environnement (IFR71), Institut National de la Santé et de la Recherche Médicale (INSERM)-Ecole Nationale Supérieure de Chimie de Paris- Chimie ParisTech-PSL (ENSCP)-Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche pour le Développement (IRD)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Ecole Nationale Supérieure de Chimie de Paris- Chimie ParisTech-PSL (ENSCP)-Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche pour le Développement (IRD)-Université Paris Descartes - Paris 5 (UPD5)-Université Paris Diderot - Paris 7 (UPD7), Unitat de Farmacologia i Farmacognòsia Facultat de Farmàcia, Nucli Universitari de Pedralbes, La Jaillière, ARVALIS - Institut du végétal [Paris], Université Pierre et Marie Curie - Paris 6 (UPMC), Institut de biologie moléculaire des plantes (IBMP), Université de Strasbourg (UNISTRA)-Centre National de la Recherche Scientifique (CNRS), Institut des sciences du végétal (ISV), Centre National de la Recherche Scientifique (CNRS), Paringa Mineração Limitada, Optimisation Thérapeutique en Neuropsychopharmacologie (VariaPsy - U1144), Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Neurobiologie des processus adaptatifs (NPA), Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS), Physiopathologie des maladies psychiatriques = Pathophysiology of Psychiatric Disorders (NPS-07), Institut du Fer à Moulin, Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Université Paris-Est Créteil Val-de-Marne - Faculté de médecine (UPEC Médecine), Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Université McGill, HAL-UPMC, Gestionnaire, Cahill, Emma [0000-0003-3054-1708], and Apollo - University of Cambridge Repository

Subjects
0301 basic medicine, Male, Dendritic spine, RNA, Untranslated, [SDV]Life Sciences [q-bio], striatum, [SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology, Dopamine, Striatum, Nucleus Accumbens, Mice, 0302 clinical medicine, Cocaine, Dopamine Uptake Inhibitors, dendritic spine, General Neuroscience, Dopaminergic, 3. Good health, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], Anatomy, Locomotion, medicine.drug, Genetically modified mouse, Histology, Presynaptic Terminals, Mice, Transgenic, Nucleus accumbens, Biology, In Vitro Techniques, Statistics, Nonparametric, 03 medical and health sciences, Glutamatergic, Imaging, Three-Dimensional, 3D imaging, medicine, Animals, Dopamine transporter, Dopamine Plasma Membrane Transport Proteins, [SCCO.NEUR]Cognitive science/Neuroscience, Dopaminergic Neurons, fungi, [SDV.NEU.NB] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology, Dendrites, Mice, Inbred C57BL, Luminescent Proteins, 030104 developmental biology, nervous system, Vesicular Monoamine Transport Proteins, Synapses, biology.protein, Neuroscience, 030217 neurology & neurosurgery
Abstract

International audience; The development of addictive behavior is associated with functional and structural plasticity in the mesocorticolimbic pathway. Increased connectivity upon cocaine administration has been inferred from increases in dendritic spine density, but without observations of presynaptic elements. Recently, we established a method that enables analyses of both dendritic spines and glutamatergic boutons and presented evidence that cocaine induces changes in striatal connectivity. As the pharmacological and behavioral effects of cocaine directly implicate dopaminergic neurons and their afferents, a remaining question is whether dopaminergic striatal innervations also undergo structural plasticity. To address this issue, we generated transgenic mice in which the fluorophore tdTomato is expressed under the promoter of the dopamine transporter gene. In these mice, specific labeling of dopaminergic boutons was observed in the striatum. Of note, the accordance of our results for control mice with previous electron microscopy studies confirms that our method can be used to decipher the spatial organization of boutons in relation to dendritic elements. Following repeated cocaine administration that led to behavioral locomotor sensitization, an increased density of dopaminergic boutons was observed 1 day later in the nucleus accumbens shell specifically, and not in other striatal regions. Combined labeling of dopaminergic boutons and striatal dendrites showed that cocaine significantly increased the percentage of dendritic spines associated with a dopaminergic bouton. Our results show that chronic cocaine administration induces structural plasticity of dopaminergic boutons that could participate in dopamine-dependent neuronal adaptations in the striatum.

Published
2017
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42. Dysfunction of homeostatic control of dopamine by astrocytes in the developing prefrontal cortex leads to cognitive impairments

Author

Petrelli, Francesco, primary, Dallérac, Glenn, additional, Pucci, Luca, additional, Calì, Corrado, additional, Zehnder, Tamara, additional, Sultan, Sébastien, additional, Lecca, Salvatore, additional, Chicca, Andrea, additional, Ivanov, Andrei, additional, Asensio, Cédric S., additional, Gundersen, Vidar, additional, Toni, Nicolas, additional, Knott, Graham William, additional, Magara, Fulvio, additional, Gertsch, Jürg, additional, Kirchhoff, Frank, additional, Déglon, Nicole, additional, Giros, Bruno, additional, Edwards, Robert H., additional, Mothet, Jean-Pierre, additional, and Bezzi, Paola, additional

Published
2018
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44. Structural and Functional Characterization of the Interaction of Snapin with the Dopamine Transporter: Differential Modulation of Psychostimulant Actions

Author

Erdozain, Amaia M, primary, De Gois, Stéphanie, additional, Bernard, Véronique, additional, Gorgievski, Victor, additional, Pietrancosta, Nicolas, additional, Dumas, Sylvie, additional, Macedo, Carlos E, additional, Vanhoutte, Peter, additional, Ortega, Jorge E, additional, Meana, J Javier, additional, Tzavara, Eleni T, additional, Vialou, Vincent, additional, and Giros, Bruno, additional

Published
2017
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45. Regulation of the Hippocampal Network by VGLUT3-Positive CCK- GABAergic Basket Cells

Author

Fasano, Caroline, primary, Rocchetti, Jill, additional, Pietrajtis, Katarzyna, additional, Zander, Johannes-Friedrich, additional, Manseau, Frédéric, additional, Sakae, Diana Y., additional, Marcus-Sells, Maya, additional, Ramet, Lauriane, additional, Morel, Lydie J., additional, Carrel, Damien, additional, Dumas, Sylvie, additional, Bolte, Susanne, additional, Bernard, Véronique, additional, Vigneault, Erika, additional, Goutagny, Romain, additional, Ahnert-Hilger, Gudrun, additional, Giros, Bruno, additional, Daumas, Stéphanie, additional, Williams, Sylvain, additional, and El Mestikawy, Salah, additional

Published
2017
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47. Deleting IGF-1 receptor from forebrain neurons confers neuroprotection during stroke and upregulates endocrine somatotropin

Author

De Magalhaes Filho, C Daniel, primary, Kappeler, Laurent, additional, Dupont, Joëlle, additional, Solinc, Julien, additional, Villapol, Sonia, additional, Denis, Cécile, additional, Nosten-Bertrand, Marika, additional, Billard, Jean-Marie, additional, Blaise, Annick, additional, Tronche, François, additional, Giros, Bruno, additional, Charriaut-Marlangue, Christiane, additional, Aïd, Saba, additional, Le Bouc, Yves, additional, and Holzenberger, Martin, additional

Published
2016
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48. Both chronic treatments by epothilone D and fluoxetine increase the short-term memory and differentially alter the mood status of STOP/MAP6 KO mice

Author

Fournet, Vincent, de Lavilléon, Gaetan, Schweitzer, Annie, Giros, Bruno, Andrieux, Annie, Martres, Marie-Pascale, INSERM U836, équipe 1, Physiopathologie du cytosquelette, Physiopathologie des Maladies du Système Nerveux Central, Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Grenoble Institut des Neurosciences (GIN), Université Joseph Fourier - Grenoble 1 (UJF)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Joseph Fourier - Grenoble 1 (UJF)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Grenoble Institut des Neurosciences (GIN), Université Joseph Fourier - Grenoble 1 (UJF)-Institut National de la Santé et de la Recherche Médicale (INSERM), Groupe Physiopathologie du Cytosquelette (GPC), Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut de Recherche Interdisciplinaire de Grenoble (IRIG), Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Direction de Recherche Fondamentale (CEA) (DRF (CEA)), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut de Recherche Interdisciplinaire de Grenoble (IRIG), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Grenoble Institut des Neurosciences (GIN), Université Joseph Fourier - Grenoble 1 (UJF)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Joseph Fourier - Grenoble 1 (UJF), Grants from INSERM and Université Pierre et Marie Curie, MENESR, and Andrieux, Annie

Subjects
antidepressant, MESH: Depression, corticosterone, serotonin/norepinephrine transporters, MESH: Affect, MESH: Mice, Knockout, MESH: Male, MESH: Memory, Short-Term, MESH: Serotonin Uptake Inhibitors, stress, MESH: Mice, 129 Strain, MESH: Microtubule-Associated Proteins, microtubule-stabilizing compound, MESH: Mice, Inbred C57BL, MESH: Antineoplastic Agents, MESH: Fluoxetine, MESH: Animals, MESH: Epothilones, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], [SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], MESH: Disease Models, Animal, anxiety/depression, MESH: Mice, MESH: Female
Abstract

International audience; Recent evidence underlines the crucial role of neuronal cytoskeleton in the pathophysiology of psychiatric diseases. In this line, the deletion of STOP/MAP6 (Stable Tubule Only Polypeptide), a microtubule-stabilizing protein, triggers various neurotransmission and behavioral defects, suggesting that STOP knockout (KO) mice could be a relevant experimental model for schizoaffective symptoms. To establish the predictive validity of such a mouse line, in which the brain serotonergic tone is dramatically imbalanced, the effects of a chronic fluoxetine treatment on the mood status of STOP KO mice were characterized. Moreover, we determined the impact, on mood, of a chronic treatment by epothilone D, a taxol-like microtubule-stabilizing compound that has previously been shown to improve the synaptic plasticity deficits of STOP KO mice. We demonstrated that chronic fluoxetine was either antidepressive and anxiolytic, or pro-depressive and anxiogenic, depending on the paradigm used to test treated mutant mice. Furthermore, control-treated STOP KO mice exhibited paradoxical behaviors, compared with their clear-cut basal mood status. Paradoxical fluoxetine effects and control-treated STOP KO behaviors could be because of their hyper-reactivity to acute and chronic stress. Interestingly, both epothilone D and fluoxetine chronic treatments improved the short-term memory of STOP KO mice. Such treatments did not affect the serotonin and norepinephrine transporter densities in cerebral areas of mice. Altogether, these data demonstrated that STOP KO mice could represent a useful model to study the relationship between cytoskeleton, mood, and stress, and to test innovative mood treatments, such as microtubule-stabilizing compounds.

Published
2012
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49. Organic cation transporter 2 controls brain norepinephrine and serotonin clearance and antidepressant response

Author

Bacq, Alexandre, Balasse, Laure, Biala, Grażyna, Guiard, Bruno, Gardier, Alain, Schinkel, Alfred, Louis, Franck, Vialou, Vincent, Martres, Marie-Pascale, Chevarin, Caroline, Hamon, Michel, Giros, Bruno, Gautron, Sophie, Gautron, Sophie, Physiopathologie des Maladies du Système Nerveux Central, Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Department of Pharmacology and Pharmacodynamics [Lublin, Poland], Medical University of Lublin [Poland], Sérotonine et neuropharmacologie, Université Paris-Sud - Paris 11 (UP11)-IFR141, Division of Molecular Biology [Amsterdam, The Netherlands], The Netherlands Cancer Institute [Amsterdam, The Netherlands], Unité de Neuropsychopharmacologie [CHU Pitié-Salpétriêre], Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), and AB, LB and VV were recipients of fellowships from the French Ministry for Research, the Société Française de Pharmacologie et Thérapeutique and the Fondation pour la Recherche Médicale. GB was a recipient of a grant from the EGIDE foundation. Financial support was provided by the Institut National pour la Santé et la Recherche Scientifique (INSERM) and the Fondation de France.

Subjects
mood, depression, antidepressant response, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], [SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], aminergic neurotransmission, organic cation transporter
Abstract

International audience; High-affinity transporters for norepinephrine (NE) and serotonin (5-HT), which ensure neurotransmitter clearance at the synapse, are the principal targets of widely used antidepressant drugs. Antidepressants targeting these high-affinity transporters, however, do not provide positive treatment outcomes for all patients. Other monoamine transport systems, with lower affinity, have been detected in the brain, but their role is largely unknown. Here we report that OCT2, a member of the polyspecific organic cation transporter (OCT) family, is expressed notably in the limbic system and implicated in anxiety and depression-related behaviors in the mouse. Genetic deletion of OCT2 in mice produced a significant reduction in brain tissue concentrations of NE and 5-HT and in ex vivo uptake of both these neurotransmitters in the presence of the dual 5-HT-NE transport blocker, venlafaxine. In vivo clearance of NE and 5-HT evaluated using microiontophoretic electrophysiology was diminished in the hippocampus of OCT2(-/-) mice in the presence of venlafaxine, thereby affecting postsynaptic neuronal activity. OCT2(-/-) mice displayed an altered sensitivity to acute treatments with NE- and/or 5-HT-selective transport blockers in the forced-swim test. Moreover, the mutant mice were insensitive to long-term venlafaxine treatment in a more realistic, corticosterone-induced, chronic depression model. Our findings identify OCT2 as an important postsynaptic determinant of aminergic tonus and mood-related behaviors and a potential pharmacological target for mood disorders therapy.

Published
2012
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50. The deletion of the microtubule-associated STOP protein affects the serotonergic mouse brain network

Author

Fournet, Vincent, Jany, Marion, Fabre, Véronique, Chali, Farah, Orsal, Didier, Schweitzer, Annie, Andrieux, Annie, Messanvi, Fany, Giros, Bruno, Hamon, Michel, Lanfumey, Laurence, Deloulme, Jean-Christophe, Martres, Marie-Pascale, Grenoble Institut des Neurosciences (GIN), Université Joseph Fourier - Grenoble 1 (UJF)-Institut National de la Santé et de la Recherche Médicale (INSERM), Physiopathologie des Maladies du Système Nerveux Central, Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Centre de Recherche de l'Institut du Cerveau et de la Moelle épinière (CRICM), Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC), Institut de psychiatrie et neurosciences (U894 / UMS 1266), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), INSERM MENESR (Paris, France), Grenoble Institut des Neurosciences ( GIN ), Institut National de la Santé et de la Recherche Médicale ( INSERM ) -CHU Grenoble-Université Joseph Fourier - Grenoble 1 ( UJF ), Université Pierre et Marie Curie - Paris 6 ( UPMC ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ), Centre de Recherche de l'Institut du Cerveau et de la Moelle épinière ( CRICM ), Centre de Psychiatrie et Neurosciences ( CPN - U894 ), Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Centre de Psychiatrie et Neurosciences (U894), and Andrieux, Annie

Subjects
MESH : Serotonin, MESH : Male, [SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology, MESH: Mice, Inbred BALB C, MESH: Mice, Knockout, MESH : Mice, 129 Strain, MESH : Maze Learning, MESH: Brain, MESH: Mice, 129 Strain, MESH : Mice, [SDV.BBM] Life Sciences [q-bio]/Biochemistry, Molecular Biology, MESH : Female, MESH: Animals, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, [ SDV.BBM ] Life Sciences [q-bio]/Biochemistry, Molecular Biology, MESH: Mice, MESH : Mice, Inbred BALB C, MESH: Maze Learning, [SDV.NEU.NB] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology, MESH: Male, MESH: Microtubule-Associated Proteins, MESH : Brain, MESH: Nerve Net, MESH : Microtubule-Associated Proteins, [ SDV.NEU.NB ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology, MESH : Nerve Net, MESH : Mice, Knockout, MESH: Serotonin, MESH : Animals, MESH: Female
Abstract

International audience; The deletion of microtubule-associated protein stable tubule only polypeptide (STOP) leads to neuroanatomical, biochemical and severe behavioral alterations in mice, partly alleviated by antipsychotics. Therefore, STOP knockout (KO) mice have been proposed as a model of some schizophrenia-like symptoms. Preliminary data showed decreased brain serotonin (5-HT) tissue levels in STOP KO mice. As literature data demonstrate various interactions between microtubule-associated proteins and 5-HT, we characterized some features of the serotonergic neurotransmission in STOP KO mice. In the brainstem, mutant mice displayed higher tissue 5-HT levels and in vivo synthesis rate, together with marked increases in 5-HT transporter densities and 5-HT1A autoreceptor levels and electrophysiological sensitivity, without modification of the serotonergic soma number. Conversely, in projection areas, STOP KO mice exhibited lower 5-HT levels and in vivo synthesis rate, associated with severe decreases in 5-HT transporter densities, possibly related to reduced serotonergic terminals. Mutant mice also displayed a deficit of adult hippocampal neurogenesis, probably related to both STOP deletion and 5-HT depletion. Finally, STOP KO mice exhibited a reduced anxiety- and, probably, an increased helpness-status, that could be because of the strong imbalance of the serotonin neurotransmission between somas and terminals. Altogether, these data suggested that STOP deletion elicited peculiar 5-HT disconnectivity.

Published
2010
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