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187 results on '"Baufreton, Jérôme"'

6. Subcellular specificity of cannabinoid effects in striatonigral circuits

Author

Soria-Gomez, Edgar, Pagano Zottola, Antonio C., Mariani, Yamuna, Desprez, Tifany, Barresi, Massimo, Bonilla-del Río, Itziar, Muguruza, Carolina, Le Bon-Jego, Morgane, Julio-Kalajzić, Francisca, Flynn, Robyn, Terral, Geoffrey, Fernández-Moncada, Ignacio, Robin, Laurie M., Oliveira da Cruz, José F., Corinti, Simone, Amer, Yasmine Ould, Goncalves, Julia, Varilh, Marjorie, Cannich, Astrid, Redon, Bastien, Zhao, Zhe, Lesté-Lasserre, Thierry, Vincent, Peggy, Tolentino-Cortes, Tarson, Busquets-García, Arnau, Puente, Nagore, Bains, Jaideep S., Hebert-Chatelain, Etienne, Barreda-Gómez, Gabriel, Chaouloff, Francis, Lohman, Alexander W., Callado, Luis F., Grandes, Pedro, Baufreton, Jerome, Marsicano, Giovanni, and Bellocchio, Luigi

Published
2021
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8. GAP43 Located on Corticostriatal Terminals Restrains Novelty-Induced Hyperactivity in Mice.

Author

Maroto, Irene B., Costas-Insua, Carlos, Montero-Fernández, Carlos, Hermoso-López, Alba, Lebouc, Margaux, Bajo-Grañeras, Raquel, Álvaro-Blázquez, Alicia, Blázquez, Cristina, Cannich, Astrid, Marsicano, Giovanni, Martín, Ricardo, Baufreton, Jérôme, Rodríguez-Crespo, Ignacio, Bellocchio, Luigi, and Guzmán, Manuel

Subjects
KNOCKOUT mice, GABAERGIC neurons, DESIGNER drugs, MENTAL illness, MEMORY disorders
Abstract

Growth-associated protein of 43 kDa (GAP43) is a key cytoskeleton-associated component of the presynaptic terminal that facilitates neuroplasticity. Downregulation of GAP43 expression has been associated to various psychiatric conditions in humans and evokes hippocampus-dependent memory impairments in mice. Despite the extensive studies conducted on hippocampal GAP43 in past decades, however, very little is known about its roles in modulating the excitatory versus inhibitory balance in other brain regions. We recently generated conditional knock-out mice in which the Gap43 gene was selectively inactivated in either telencephalic glutamatergic neurons (Gap43fl/fl ; Nex1Cre mice, hereafter Glu-GAP43-/- mice) or forebrain GABAergic neurons (Gap43fl/fl; Dlx5/6Cre mice, hereafter GABA-GAP43-/- mice). Here, we show that Glu-GAP43-/- but not GABA-GAP43-/-mice of either sex show a striking hyperactive phenotype when exposed to a novel environment. This behavioral alteration of Glu-GAP43-/- mice was linked to a selective activation of dorsal-striatum neurons, as well as to an enhanced corticostriatal glutamatergic transmission and an abrogation of corticostriatal endocannabinoid-mediated long-term depression. In line with these observations, GAP43 was abundantly expressed in corticostriatal glutamatergic terminals of wild-type mice. The novelty-induced hyperactive phenotype of Glu-GAP43-/- mice was abrogated by chemogenetically inhibiting corticostriatal afferences with a Gi-coupled "designer receptor exclusively activated by designer drugs" (DREADDs), thus further supporting that novelty-induced activity is controlled by GAP43 at corticostriatal excitatory projections. Taken together, these findings show an unprecedented regulatory role of GAP43 in the corticostriatal circuitry and provide a new mouse model with a delimited neuronal-circuit alteration for studying novelty-induced hyperactivity, a phenotypic shortfall that occurs in diverse psychiatric diseases. [ABSTRACT FROM AUTHOR]

Published
2024
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18. A physiologically realistic computational model of the basal ganglia network

Author

Azevedo Carvalho, Nathalie, Buhry, Laure, Contassot-Vivier, Sylvain, Baufreton, Jérôme, Martinez, Dominique, AZEVEDO CARVALHO, Nathalie, Analysis and modeling of neural systems by a system neuroscience approach (NEUROSYS), Inria Nancy - Grand Est, Institut National de Recherche en Informatique et en Automatique (Inria)-Institut National de Recherche en Informatique et en Automatique (Inria)-Department of Complex Systems, Artificial Intelligence & Robotics (LORIA - AIS), Laboratoire Lorrain de Recherche en Informatique et ses Applications (LORIA), Institut National de Recherche en Informatique et en Automatique (Inria)-Université de Lorraine (UL)-Centre National de la Recherche Scientifique (CNRS)-Institut National de Recherche en Informatique et en Automatique (Inria)-Université de Lorraine (UL)-Centre National de la Recherche Scientifique (CNRS)-Laboratoire Lorrain de Recherche en Informatique et ses Applications (LORIA), Institut National de Recherche en Informatique et en Automatique (Inria)-Université de Lorraine (UL)-Centre National de la Recherche Scientifique (CNRS)-Université de Lorraine (UL)-Centre National de la Recherche Scientifique (CNRS), SIMulating and Building IOT (SIMBIOT), Department of Networks, Systems and Services (LORIA - NSS), Institut National de Recherche en Informatique et en Automatique (Inria)-Université de Lorraine (UL)-Centre National de la Recherche Scientifique (CNRS)-Institut National de Recherche en Informatique et en Automatique (Inria)-Université de Lorraine (UL)-Centre National de la Recherche Scientifique (CNRS), Université de Bordeaux (UB), Institut des Maladies Neurodégénératives [Bordeaux] (IMN), Université de Bordeaux (UB)-Centre National de la Recherche Scientifique (CNRS), CNRS, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France., Département Biorobotique, ISM, CNRS, F-13009 Marseille, France, Institut des Sciences du Mouvement, CNRS, F-13009 Marseille, France, Institut des Sciences du Mouvement Etienne Jules Marey (ISM), and Aix Marseille Université (AMU)-Centre National de la Recherche Scientifique (CNRS)

Subjects
Physiological realistic model, [SCCO.NEUR]Cognitive science/Neuroscience, [SCCO.NEUR] Cognitive science/Neuroscience, Basal ganglia, [INFO.INFO-MO] Computer Science [cs]/Modeling and Simulation, [INFO.INFO-BI]Computer Science [cs]/Bioinformatics [q-bio.QM], [INFO.INFO-MO]Computer Science [cs]/Modeling and Simulation, Neuroscience, [INFO.INFO-BI] Computer Science [cs]/Bioinformatics [q-bio.QM]
Abstract

International audience; The basal ganglia (BG) are a set of nuclei that process movement information: they refine and adjust simple movement actions. The BG has two major pathways: the striatum (STR)-indirect neuron pathway and the subthalamic (STN)-hyperdirect nucleus pathway. The GPe is the connecting nucleus between the two pathways. The STR inhibits the GPe and the STN excites the GPe which is divided into two types of neurons [1, 4], the prototypical and the arkypallidal. This discovery allows for a better understanding of the functioning of this neural network. We model the STN-GPeA-GPeP-STR(D2) network and study the influence of the nucleus on each other like in [2]. The neurons have been modeled as point neurons using the Hodgkin-Huxley formalism and the synapses as exponential functions. From extensive simulations performed with the SiReNe software (Neural network simulator, in french: Simulateur de Réseaux de Neurones [3]), we show that our network is in good agreement with the physiological results of [2]. This simulator is based on a hybrid method combining time-step and event-driven computations with a Runge-Kutta numerical method at inner level. GPe is mainly inhibited by GABAergic inputs ofthe STR and we study the impact of STR connectivity on GPe. We observe that the GPeP and GPeA react in opposite ways when the STR is activated, i.e. GPeP is entirely inhibited whereas the GPeA and STN are completely excited, as observed in [2]. This work aims at better understanding the synaptic connectivity scheme. This model will allow us to test hypotheses regarding the pathological rhythmogenesis in Parkinson disease, both at the cellular and connectivity levels.

Published
2021

19. A computational model of GPe prototypic and arkypallidal neurons with automated parameter fitting

Author

Azevedo Carvalho, Nathalie, Buhry, Laure, Contassot-Vivier, Sylvain, Baufreton, Jérôme, Martinez, Dominique, AZEVEDO CARVALHO, Nathalie, Analysis and modeling of neural systems by a system neuroscience approach (NEUROSYS), Inria Nancy - Grand Est, Institut National de Recherche en Informatique et en Automatique (Inria)-Institut National de Recherche en Informatique et en Automatique (Inria)-Department of Complex Systems, Artificial Intelligence & Robotics (LORIA - AIS), Laboratoire Lorrain de Recherche en Informatique et ses Applications (LORIA), Institut National de Recherche en Informatique et en Automatique (Inria)-Université de Lorraine (UL)-Centre National de la Recherche Scientifique (CNRS)-Institut National de Recherche en Informatique et en Automatique (Inria)-Université de Lorraine (UL)-Centre National de la Recherche Scientifique (CNRS)-Laboratoire Lorrain de Recherche en Informatique et ses Applications (LORIA), Institut National de Recherche en Informatique et en Automatique (Inria)-Université de Lorraine (UL)-Centre National de la Recherche Scientifique (CNRS)-Université de Lorraine (UL)-Centre National de la Recherche Scientifique (CNRS), SIMulating and Building IOT (SIMBIOT), Department of Networks, Systems and Services (LORIA - NSS), Institut National de Recherche en Informatique et en Automatique (Inria)-Université de Lorraine (UL)-Centre National de la Recherche Scientifique (CNRS)-Institut National de Recherche en Informatique et en Automatique (Inria)-Université de Lorraine (UL)-Centre National de la Recherche Scientifique (CNRS), Université de Bordeaux (UB), Institut des Maladies Neurodégénératives [Bordeaux] (IMN), Université de Bordeaux (UB)-Centre National de la Recherche Scientifique (CNRS), CNRS, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France., Département Biorobotique, ISM, CNRS, F-13009 Marseille, France, Institut des Sciences du Mouvement, CNRS, F-13009 Marseille, France, Institut des Sciences du Mouvement Etienne Jules Marey (ISM), and Aix Marseille Université (AMU)-Centre National de la Recherche Scientifique (CNRS)

Subjects
[SCCO.NEUR]Cognitive science/Neuroscience, Computational model, [SCCO.NEUR] Cognitive science/Neuroscience, [INFO.INFO-MO] Computer Science [cs]/Modeling and Simulation, [INFO.INFO-BI]Computer Science [cs]/Bioinformatics [q-bio.QM], Parameter fitting, [INFO.INFO-MO]Computer Science [cs]/Modeling and Simulation, GPeA/ GPeP neurons, Neuroscience, [INFO.INFO-BI] Computer Science [cs]/Bioinformatics [q-bio.QM]
Abstract

International audience; Parkinson’s disease is characterized by pathological oscillations in the basal ganglia. To gain insight on the origin of these oscillations, we developed a computational model of the globus pallidus (GPe). Our model consists of interconnected prototypic (GPeP) and arkypallidal (GPeA) neurons [1, 5]. We modeled GPeP and GPeA neurons as single-compartment neurons using Hodgkin-Huxley formalism. The GPeA and GPeP neurons have similar ionic currents (I_NaP, I_NaF, I_HCN, I_SK, I_Kv3, I_Ca2+, I_leak) but differ from their conductance values. We tuned the parameters automatically with a multi-objective optimization approach, a variant of the differential evolution [4, 6]. From extensive simulations performed with the SiReNe software (Neural networks simulator, in french: Simulateur de Réseaux de Neurones [3]), we show that our model of GPeP and GPeA neurons are in good agreement with the physiological results of [1], i.e. F-I curves (see Fig. 1A), Voltage-Clamp and I-V relation (see Fig. 1B,C), shape of Action Potentials. Moreover, we show that our GPeP/A neurons interconnected with GABAergic synapses exhibit activity patterns similar to those observed in vivo [2]. This work aims at better understanding the influence of these two different types of neurons in Parkinson’s disease.

Published
2021

25. Inhibition of striatonigral autophagy as a link between cannabinoid intoxication and impairment of motor coordination

Author

Blázquez, Cristina, primary, Ruiz-Calvo, Andrea, additional, Bajo-Grañeras, Raquel, additional, Baufreton, Jérôme M, additional, Resel, Eva, additional, Varilh, Marjorie, additional, Pagano Zottola, Antonio C, additional, Mariani, Yamuna, additional, Cannich, Astrid, additional, Rodríguez-Navarro, José A, additional, Marsicano, Giovanni, additional, Galve-Roperh, Ismael, additional, Bellocchio, Luigi, additional, and Guzmán, Manuel, additional

Published
2020
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26. A disynaptic circuit in the globus pallidus controls locomotion inhibition

Author

Aristieta, Asier, primary, Barresi, Massimo, additional, Lindi, Shiva A., additional, Barriere, Gregory, additional, Courtand, Gilles, additional, de la Crompe, Brice, additional, Guilhemsang, Lise, additional, Gauthier, Sophie, additional, Fioramonti, Stéphanie, additional, Baufreton, Jérôme, additional, and Mallet, Nicolas P., additional

Published
2020
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27. Author response: Inhibition of striatonigral autophagy as a link between cannabinoid intoxication and impairment of motor coordination

Author

Blázquez, Cristina, primary, Ruiz-Calvo, Andrea, additional, Bajo-Grañeras, Raquel, additional, Baufreton, Jérôme M, additional, Resel, Eva, additional, Varilh, Marjorie, additional, Pagano Zottola, Antonio C, additional, Mariani, Yamuna, additional, Cannich, Astrid, additional, Rodríguez-Navarro, José A, additional, Marsicano, Giovanni, additional, Galve-Roperh, Ismael, additional, Bellocchio, Luigi, additional, and Guzmán, Manuel, additional

Published
2020
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32. Cellular and Synaptic Dysfunctions in Parkinson’s Disease: Stepping out of the Striatum

Author

Mallet, Nicolas, Delgado, Lorena, Chazalon, Marine, Miguelez, Cristina, Baufreton, Jérôme, Institut des Maladies Neurodégénératives [Bordeaux] (IMN), and Université de Bordeaux (UB)-Centre National de la Recherche Scientifique (CNRS)

Subjects
subthalamic nucleus, nervous system, substantia nigra, lcsh:Biology (General), [SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology, Globus pallidus, pacemaking, dopamine, neuronal excitability, GABAergic transmission, neuronal oscillations, lcsh:QH301-705.5, ComputingMilieux_MISCELLANEOUS
Abstract

The basal ganglia (BG) are a collection of interconnected subcortical nuclei that participate in a great variety of functions, ranging from motor programming and execution to procedural learning, cognition, and emotions. This network is also the region primarily affected by the degeneration of midbrain dopaminergic neurons localized in the substantia nigra pars compacta (SNc). This degeneration causes cellular and synaptic dysfunctions in the BG network, which are responsible for the appearance of the motor symptoms of Parkinson’s disease. Dopamine (DA) modulation and the consequences of its loss on the striatal microcircuit have been extensively studied, and because of the discrete nature of DA innervation of other BG nuclei, its action outside the striatum has been considered negligible. However, there is a growing body of evidence supporting functional extrastriatal DA modulation of both cellular excitability and synaptic transmission. In this review, the functional relevance of DA modulation outside the striatum in both normal and pathological conditions will be discussed.

Published
2019
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33. Cellular and Synaptic Dysfunctions in Parkinson's Disease: Stepping Out of the Striatum

Author

Farmacología, Farmakologia, Mallet, Nicolas, Delgado Zabalza, Lorena, Chazalon, Marine, Miguélez Palomo, Cristina, Baufreton, Jérôme, Farmacología, Farmakologia, Mallet, Nicolas, Delgado Zabalza, Lorena, Chazalon, Marine, Miguélez Palomo, Cristina, and Baufreton, Jérôme

Abstract

The basal ganglia (BG) are a collection of interconnected subcortical nuclei that participate in a great variety of functions, ranging from motor programming and execution to procedural learning, cognition, and emotions. This network is also the region primarily affected by the degeneration of midbrain dopaminergic neurons localized in the substantia nigra pars compacta (SNc). This degeneration causes cellular and synaptic dysfunctions in the BG network, which are responsible for the appearance of the motor symptoms of Parkinson's disease. Dopamine (DA) modulation and the consequences of its loss on the striatal microcircuit have been extensively studied, and because of the discrete nature of DA innervation of other BG nuclei, its action outside the striatum has been considered negligible. However, there is a growing body of evidence supporting functional extrastriatal DA modulation of both cellular excitability and synaptic transmission. In this review, the functional relevance of DA modulation outside the striatum in both normal and pathological conditions will be discussed.

Published
2019

35. Inhaling xenon ameliorates l -dopa-induced dyskinesia in experimental parkinsonism

Author

Baufreton, Jérôme, Milekovic, Tomislav, Li, Qin, McGuire, Steve, Moraud, Eduardo Martin, Porras, Gregory, Sun, Shiqi, Ko, Wai Kin D., Chazalon, Marine, Morin, Stephanie, Normand, Elisabeth, Farjot, Géraldine, Milet, Aude, Pype, Jan, Pioli, Elsa, Courtine, Grégoire, Bessière, Baptiste, Bezard, Erwan, Neurodegeneratives Diseases Institute (IMN-UMR CNRS 5293), Centre National de la Recherche Scientifique (CNRS), Institut des Maladies Neurodégénératives [Bordeaux] (IMN), Université de Bordeaux (UB)-Centre National de la Recherche Scientifique (CNRS), IMN (UMR 5293), Center for Neuroprosthetics and Brain Mind Institute, School of Life Sciences, Swiss Federal Institute of Technology (EPFL), Institute of Lab Animal Sciences, China Academy of Medical Sciences, Beijing, China, China Academy of Medical Sciences, Beijing, China, Motac Neuroscience, Manchester, United Kingdom., Motac Neuroscience, Bertarelli Foundation Chair in Translational Neuroengineering, Ecole Polytechnique Fédérale de Lausanne (EPFL)- Center for Neuroprosthetics and Institute of Bioengineering, Institut Interdisciplinaire des Neurosciences de Bordeaux, Génétique moléculaire, neurophysiologie et comportement, School of Computer Engineering, and Nanyang Technological University [Singapour]

Subjects
[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology, otorhinolaryngologic diseases, ComputingMilieux_MISCELLANEOUS, nervous system diseases
Abstract

Parkinson's disease motor symptoms are treated with levodopa, but long‐term treatment leads to disabling dyskinesia. Altered synaptic transmission and maladaptive plasticity of corticostriatal glutamatergic projections play a critical role in the pathophysiology of dyskinesia. Because the noble gas xenon inhibits excitatory glutamatergic signaling, primarily through allosteric antagonism of the N‐methyl‐d‐aspartate receptors, we aimed to test its putative antidyskinetic capabilities. We first studied the direct effect of xenon gas exposure on corticostriatal plasticity in a murine model of levodopa‐induced dyskinesia We then studied the impact of xenon inhalation on behavioral dyskinetic manifestations in the gold‐standard rat and primate models of PD and levodopa‐induced dyskinesia. Last, we studied the effect of xenon inhalation on axial gait and posture deficits in a primate model of PD with levodopa‐induced dyskinesia. This study shows that xenon gas exposure (1) normalized synaptic transmission and reversed maladaptive plasticity of corticostriatal glutamatergic projections associated with levodopa‐induced dyskinesia, (2) ameliorated dyskinesia in rat and nonhuman primate models of PD and dyskinesia, and (3) improved gait performance in a nonhuman primate model of PD. These results pave the way for clinical testing of this unconventional but safe approach. © 2018 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society

Published
2018
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38. D5 dopamine receptors control glutamatergic AMPA transmission between the motor cortex and subthalamic nucleus

Author

Farmacología, Farmakologia, Froux, Lionel, Le Bon-Jego, Morgane, Miguélez Palomo, Cristina, Normand, Elisabeth, Morin, Stephanie, Fioramonti, Stéphanie, Barresi, Massimo, Frick, Andreas, Baufreton, Jérôme, Taupignon, Anne, Farmacología, Farmakologia, Froux, Lionel, Le Bon-Jego, Morgane, Miguélez Palomo, Cristina, Normand, Elisabeth, Morin, Stephanie, Fioramonti, Stéphanie, Barresi, Massimo, Frick, Andreas, Baufreton, Jérôme, and Taupignon, Anne

Abstract

Corticofugal fibers target the subthalamic nucleus (STN), a component nucleus of the basal ganglia, in addition to the striatum, their main input. The cortico-subthalamic, or hyperdirect, pathway, is thought to supplement the cortico-striatal pathways in order to interrupt/change planned actions. To explore the previously unknown properties of the neurons that project to the STN, retrograde and anterograde tools were used to specifically identify them in the motor cortex and selectively stimulate their synapses in the STN. The cortico-subthalamic neurons exhibited very little sag and fired an initial doublet followed by non-adapting action potentials. In the STN, AMPA/kainate synaptic currents had a voltage-dependent conductance, indicative of GluA2-lacking receptors and were partly inhibited by Naspm. AMPA transmission displayed short-term depression, with the exception of a limited bandpass in the 5 to 15 Hz range. AMPA synaptic currents were negatively controlled by dopamine D5 receptors. The reduction in synaptic strength was due to postsynaptic D5 receptors, mediated by a PKA-dependent pathway, but did not involve a modified rectification index. Our data indicated that dopamine, through post-synaptic D5 receptors, limited the cortical drive onto STN neurons in the normal brain.

Published
2018

39. GAT-3 Dysfunction Generates Tonic Inhibition in Exter nal Globus Pallidus Neurons in Parkinsonian Rodents

Author

Farmacología, Farmakologia, Chazalon, Marine, Paredes Rodríguez, Elena, Morin, Stéphanie, Martinez, Audrey, Cristóvão-Ferreira, Sofia, Vaz, Sandra, Sebastiao, Ana, Panatier, Aude, Boué-Grabot, Eric, Miguélez Palomo, Cristina, Baufreton, Jérôme, Farmacología, Farmakologia, Chazalon, Marine, Paredes Rodríguez, Elena, Morin, Stéphanie, Martinez, Audrey, Cristóvão-Ferreira, Sofia, Vaz, Sandra, Sebastiao, Ana, Panatier, Aude, Boué-Grabot, Eric, Miguélez Palomo, Cristina, and Baufreton, Jérôme

Abstract

The external globus pallidus (GP) is a key GABAergic hub in the basal ganglia (BG) circuitry, a neuronal network involved in motor control. In Parkinson's disease (PD), the rate and pattern of activity of GP neurons are profoundly altered and contribute to the motor symptoms of the disease. In rodent models of PD, the striato-pallidal pathway is hyperactive, and extracellular GABA concentrations are abnormally elevated in the GP, supporting the hypothesis of an alteration of neuronal and/or glial clearance of GABA. Here, we discovered the existence of persistent GABAergic tonic inhibition in GP neurons of dopamine-depleted (DD) rodent models. We showed that glial GAT-3 transporters are down-regulated while neuronal GAT-1 function remains normal in DD rodents. Finally, we showed that blocking GAT-3 activity in vivo alters the motor coordination of control rodents, suggesting that GABAergic tonic inhibition in the GP contributes to the pathophysiology of PD.

Published
2018

40. Alteration of GABAergic neurotransmission in Huntington's disease

Author

Garret, Maurice, Du, Zhuowei, Chazalon, Marine, Cho, Yoon H., Baufreton, Jérôme, Garret, Maurice, Du, Zhuowei, Chazalon, Marine, Cho, Yoon H., and Baufreton, Jérôme

Abstract

Hereditary Huntington's disease (HD) is characterized by cell dysfunction and death in the brain, leading to progressive cognitive, psychiatric, and motor impairments. Despite molecular and cellular descriptions of the effects of the HD mutation, no effective pharmacological treatment is yet available. In addition to well-established alterations of glutamatergic and dopaminergic neurotransmitter systems, it is becoming clear that the GABAergic systems are also impaired in HD. GABA is the major inhibitory neurotransmitter in the brain, and GABAergic neurotransmission has been postulated to be modified in many neurological and psychiatric diseases. In addition, GABAergic neurotransmission is the target of many drugs that are in wide clinical use. Here, we summarize data demonstrating the occurrence of alterations of GABAergic markers in the brain of HD carriers as well as in rodent models of the disease. In particular, we pinpoint HD-related changes in the expression of GABAA receptors (GABAARs). On the basis that a novel GABA pharmacology of GABAARs established with more selective drugs is emerging, we argue that clinical treatments acting specifically on GABAergic neurotransmission may be an appropriate strategy for improving symptoms linked to the HD mutation., SCOPUS: re.j, info:eu-repo/semantics/published

Published
2018

42. Prototypic and Arkypallidal Neurons in the Dopamine-Intact External Globus Pallidus

Author

Abdi, Azzedine, Mallet, Nicolas, Mohamed, Foad Y, Sharott, Andrew, Dodson, Paul D, Nakamura, Kouichi C, Suri, Sana, Avery, Sophie V, Larvin, Joseph T, Garas, Farid N, Garas, Shady N, Vinciati, Federica, Morin, Stéphanie, Bezard, Erwan, Baufreton, Jérôme, Magill, Peter J, Institut des Maladies Neurodégénératives [Bordeaux] (IMN), Université de Bordeaux (UB)-Centre National de la Recherche Scientifique (CNRS), and University of Oxford [Oxford]

Subjects
anatomy, [SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology, Dopamine, Green Fluorescent Proteins, Thyroid Nuclear Factor 1, Action Potentials, ELAV-Like Protein 3, In Vitro Techniques, Globus Pallidus, Statistics, Nonparametric, Adrenergic Agents, Subthalamic Nucleus, Neural Pathways, Animals, Oxidopamine, transcription factor, Neurons, Nuclear Proteins, Forkhead Transcription Factors, Articles, electrophysiology, arkypallidal, Rats, Parvalbumins, nervous system, Animals, Newborn, ELAV Proteins, basal ganglia, Female, Transcription Factors
Abstract

International audience; Studies in dopamine-depleted rats indicate that the external globus pallidus (GPe) contains two main types of GABAergic projection cell; so-called "prototypic" and "arkypallidal" neurons. Here, we used correlative anatomical and electrophysiological approaches in rats to determine whether and how this dichotomous organization applies to the dopamine-intact GPe. Prototypic neurons coexpressed the transcription factors Nkx2-1 and Lhx6, comprised approximately two-thirds of all GPe neurons, and were the major GPe cell type innervating the subthalamic nucleus (STN). In contrast, arkypallidal neurons expressed the transcription factor FoxP2, constituted just over one-fourth of GPe neurons, and innervated the striatum but not STN. In anesthetized dopamine-intact rats, molecularly identified prototypic neurons fired at relatively high rates and with high regularity, regardless of brain state (slow-wave activity or spontaneous activation). On average, arkypallidal neurons fired at lower rates and regularities than prototypic neurons, and the two cell types could be further distinguished by the temporal coupling of their firing to ongoing cortical oscillations. Complementing the activity differences observed in vivo, the autonomous firing of identified arkypallidal neurons in vitro was slower and more variable than that of prototypic neurons, which tallied with arkypallidal neurons displaying lower amplitudes of a "persistent" sodium current important for such pacemaking. Arkypallidal neurons also exhibited weaker driven and rebound firing compared with prototypic neurons. In conclusion, our data support the concept that a dichotomous functional organization, as actioned by arkypallidal and prototypic neurons with specialized molecular, structural, and physiological properties, is fundamental to the operations of the dopamine-intact GPe.

Published
2015
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48. l-DOPA Impairs Proteasome Activity in Parkinsonism through D1Dopamine Receptor

Author

Berthet, Amandine, primary, Bezard, Erwan, additional, Porras, Gregory, additional, Fasano, Stefania, additional, Barroso-Chinea, Pedro, additional, Dehay, Benjamin, additional, Martinez, Audrey, additional, Thiolat, Marie-Laure, additional, Nosten-Bertrand, Marika, additional, Giros, Bruno, additional, Baufreton, Jérôme, additional, Li, Qin, additional, Bloch, Bertrand, additional, and Martin-Negrier, Marie-Laure, additional

Published
2012
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