
Membres de l'équipe
Thomas Rival
Cellular Interactions, Neurodegeneration and Neuroplasticity
We investigate the organization and functional dynamics of brain neuronal circuits, their adaptive capacities and the mechanisms underlying their pathological dysfunction and neurodegeneration, with focus onto the basal ganglia network.
Notre principal intérêt de recherche porte sur la transmission synaptique, la neurodégénération et la neuroplasticité dans le cerveau adulte. La communication entre les neurones au niveau de leurs connexions, appelées synapses, est le substrat du traitement de l’information dans les réseaux qui sous-tendent les fonctions cérébrales. La transmission synaptique est un processus hautement dynamique et régulé, influencé par les cellules gliales, dont les anomalies sont associées à un certain nombre de maladies cérébrales (notion de synaptopathies). Neurodégénérescence est un processus pathologique qui déclenche le dysfonctionnement et la mort progressive des cellules nerveuses. La compréhension des mécanismes pathologiques qui déclenchent et entretiennent la neurodégénérescence (pathogenèse), de ses conséquences sur le fonctionnement des circuits et des mécanismes qui aident les neurones à gérer le stress cellulaire est essentielle pour le développement de traitements curatifs ou modificateurs de la maladie pour les troubles neurodégénératifs dévastateurs, tels que la maladie de Parkinson (MP). Neuroplasticité. désigne la capacité du système nerveux à s’adapter en réponse à l’expérience et aux stimulations internes ou externes en modifiant les interactions entre les cellules nerveuses, y compris les changements dans le nombre de synapses et l’efficacité/la force de la transmission synaptique (plasticité synaptique), ou en générant de nouvelles cellules nerveuses. Cette faculté n’est pas limitée au développement, mais se produit tout au long de la vie, bien qu’elle diminue avec le vieillissement. La neuroplasticité a notamment été impliquée dans les processus d’apprentissage et de mémoire. Elle se produit également dans des conditions pathologiques ou en réponse à des traitements chroniques. Ces changements adaptatifs peuvent représenter des mécanismes compensatoires contrecarrant les déficits déclenchés par le dysfonctionnement ou la mort neuronale, retardant l’apparition des symptômes, ou, au contraire, participer à ces déficits, voire les aggraver.
L’équipe étudie ces processus dans le contexte des fonctions et des pathologies liées aux ganglions de la base (BG), en particulier la MP, un trouble du mouvement caractérisé par la dégénérescence des neurones dopaminergiques du mésencéphale innervant le striatum, la principale station d’entrée des BG. Par le biais de collaborations, nos travaux abordent également des questions fondamentales et cliniquement pertinentes dans le contexte d’autres neuropathologies, notamment les troubles du spectre autistique (TSA), la maladie d’Alzheimer et la maladie de Charcot-Marie-Tooth.
Publications
Cholinergic interneuron inhibition potentiates corticostriatal transmission in direct medium spiny neurons and rescues motor learning in parkinsonism
TP53INP1 exerts neuroprotection under ageing and Parkinson’s disease-related stress condition
Glutamate transporter 1-expressing glia in the rat substantia nigra-Morphometric analysis and relationships to synapses
Postnatal Tshz3 Deletion Drives Altered Corticostriatal Function and Autism Spectrum Disorder-like Behavior
TSHZ3 deletion causes an autism syndrome and defects in cortical projection neurons
Striatal Cholinergic Interneurons Control Motor Behavior and Basal Ganglia Function in Experimental Parkinsonism
Cholinergic interneuron inhibition potentiates corticostriatal transmission in direct medium spiny neurons and rescues motor learning in parkinsonism
Processing of information from the parafascicular nucleus of the thalamus through the basal ganglia
Targeted Tshz3 deletion in corticostriatal circuit components segregates core autistic behaviors
Postsynaptic autism spectrum disorder genes and synaptic dysfunction
A stable proportion of Purkinje cell inputs from parallel fibers are silent during cerebellar maturation
Camk2a-Cre and Tshz3 Expression in Mouse Striatal Cholinergic Interneurons: Implications for Autism Spectrum Disorder
TP53INP1 exerts neuroprotection under ageing and Parkinson’s disease-related stress condition
Golgi staining-like retrograde labeling of brain circuits using rabies virus: Focus onto the striatonigral neurons
Reply to: Letter to the Editor by MartÃnez-Fernández
Subthalamic Nucleus Stimulation Impairs Motivation: Implication for Apathy in Parkinson’s Disease
Glutamate transporter 1-expressing glia in the rat substantia nigra-Morphometric analysis and relationships to synapses
Construct Validity and Cross Validity of a Test Battery Modeling Autism Spectrum Disorder (ASD) in Mice.
Striatal Cholinergic Interneurons: How to Elucidate Their Function in Health and Disease
Postnatal Tshz3 Deletion Drives Altered Corticostriatal Function and Autism Spectrum Disorder-like Behavior
Opto nongenetics inhibition of neuronal firing
Chronic fornix deep brain stimulation in a transgenic Alzheimer’s rat model reduces amyloid burden, inflammation, and neuronal loss
TSHZ3 deletion causes an autism syndrome and defects in cortical projection neurons
Involvement of Striatal Cholinergic Interneurons and M1 and M4 Muscarinic Receptors in Motor Symptoms of Parkinson’s Disease.
SLC35D3 increases autophagic activity in midbrain dopaminergic neurons by enhancing BECN1-ATG14-PIK3C3 complex formation
LAMP5 Fine-Tunes GABAergic Synaptic Transmission in Defined Circuits of the Mouse Brain.
Metabolic, synaptic and behavioral impact of 5-week chronic deep brain stimulation in hemiparkinsonian rats.
Synaptic scaling up in medium spiny neurons of aged BACHD mice: A slow-progression model of Huntington’s disease
Endocannabinoids Mediate Muscarinic Acetylcholine Receptor-Dependent Long-Term Depression in the Adult Medial Prefrontal Cortex
Bee Venom Alleviates Motor Deficits and Modulates the Transfer of Cortical Information through the Basal Ganglia in Rat Models of Parkinson’s Disease
Striatal Cholinergic Interneurons Control Motor Behavior and Basal Ganglia Function in Experimental Parkinsonism
Differential organization of cortical inputs to striatal projection neurons of the matrix compartment in rats.
Progressive brain metabolic changes under deep brain stimulation of subthalamic nucleus in parkinsonian rats.
Oxygen glucose deprivation-induced astrocyte dysfunction provokes neuronal death through oxidative stress.
Cellular and Behavioral Outcomes of Dorsal Striatonigral Neuron Ablation: New Insights into Striatal Functions.
Distinct effects of mGlu4 receptor positive allosteric modulators at corticostriatal vs. striatopallidal synapses may differentially contribute to their antiparkinsonian action.
Tyrosine hydroxylase expression and activity in nigrostriatal dopaminergic neurons of MPTP-treated mice at the presymptomatic and symptomatic stages of parkinsonism
Progressive Parkinsonism by acute dysfunction of excitatory amino acid transporters in the rat substantia nigra
Spatial learning, monoamines and oxidative stress in rats exposed to 900 MHz electromagnetic field in combination with iron overload
Striatal molecular signature of subchronic subthalamic nucleus high frequency stimulation in parkinsonian rat.
Synergy between L-DOPA and a novel positive allosteric modulator of metabotropic glutamate receptor 4: implications for Parkinson’s disease treatment and dyskinesia.
The nucleus accumbens 5-HTRâ‚„-CART pathway ties anorexia to hyperactivity.
The nucleus accumbens 5-HTRâ‚„-CART pathway ties anorexia to hyperactivity.
Portable microstimulator for chronic deep brain stimulation in freely moving rats.
Antiparkinsonian action of a selective group III mGlu receptor agonist is associated with reversal of subthalamonigral overactivity.
High frequency stimulation of the subthalamic nucleus impacts adult neurogenesis in a rat model of Parkinson’s disease.
The added value of rabies virus as a retrograde tracer when combined with dual anterograde tract-tracing.
Deep brain stimulation mechanisms: beyond the concept of local functional inhibition.
Forelimb dyskinesia mediated by high-frequency stimulation of the subthalamic nucleus is linked to rapid activation of the NR2B subunit of N-methyl-D-aspartate receptors.
Deep brain stimulation of the center median-parafascicular complex of the thalamus has efficient anti-parkinsonian action associated with widespread cellular responses in the basal ganglia network in a rat model of Parkinson’s disease.
[Acetylcholinesterase inhibitors in Alzheimer’s disease: further comments on their mechanisms of action and therapeutic consequences].
Enhancement of L-3-hydroxybutyryl-CoA dehydrogenase activity and circulating ketone body levels by pantethine. Relevance to dopaminergic injury.
Effects of GPi and STN inactivation on physiological, motor, cognitive and motivational processes in animal models of Parkinson’s disease.
Downstream mechanisms triggered by mitochondrial dysfunction in the basal ganglia: from experimental models to neurodegenerative diseases.
Ciliary neurotrophic factor protects striatal neurons against excitotoxicity by enhancing glial glutamate uptake.
Rationale for targeting the thalamic centre-median parafascicular complex in the surgical treatment of Parkinson’s disease.
Cocaine-induced stereotypy is linked to an imbalance between the medial prefrontal and sensorimotor circuits of the basal ganglia.
Electrophysiological and behavioral evidence that modulation of metabotropic glutamate receptor 4 with a new agonist reverses experimental parkinsonism.
Different functional basal ganglia subcircuits associated with anti-akinetic and dyskinesiogenic effects of antiparkinsonian therapies.
Mechanisms contributing to the phase-dependent regulation of neurogenesis by the novel antidepressant, agomelatine, in the adult rat hippocampus.
Deep brain stimulation in neurological diseases and experimental models: from molecule to complex behavior.
Changes to interneuron-driven striatal microcircuits in a rat model of Parkinson’s disease.
Metabotropic glutamate receptor subtype 4 selectively modulates both glutamate and GABA transmission in the striatum: implications for Parkinson’s disease treatment.
Role of glutamate transporters in corticostriatal synaptic transmission.
Impact of surgery targeting the caudal intralaminar thalamic nuclei on the pathophysiological functioning of basal ganglia in a rat model of Parkinson’s disease.
Importance of circadian rhythmicity in the cholinergic treatment of Alzheimer’s disease: focus on galantamine*.
High-resolution neuroanatomical tract-tracing for the analysis of striatal microcircuits.
Plasma membrane expression of the neuronal glutamate transporter EAAC1 is regulated by glial factors: evidence for different regulatory pathways associated with neuronal maturation.
Preferential vulnerability of mesencephalic dopamine neurons to glutamate transporter dysfunction.
Na(v)1.7 and Na(v)1.3 are the only tetrodotoxin-sensitive sodium channels expressed by the adult guinea pig enteric nervous system.
High-frequency stimulation of the subthalamic nucleus potentiates L-DOPA-induced neurochemical changes in the striatum in a rat model of Parkinson’s disease.
Deficits of glutamate transmission in the striatum of experimental hemiballism.
Chronic high-frequency stimulation of the subthalamic nucleus and L-DOPA treatment in experimental parkinsonism: effects on motor behaviour and striatal glutamate transmission.
The neuronal excitatory amino acid transporter EAAC1/EAAT3: does it represent a major actor at the brain excitatory synapse?
Glutamate leakage from a compartmentalized intracellular metabolic pool and activation of the lipoxygenase pathway mediate oxidative astrocyte death by reversed glutamate transport.
Ciliary neurotrophic factor activates astrocytes, redistributes their glutamate transporters GLAST and GLT-1 to raft microdomains, and improves glutamate handling in vivo.
Transient hippocampal down-regulation of Kv1.1 subunit mRNA during associative learning in rats.
Enhanced delivery of gamma-secretase inhibitor DAPT into the brain via an ascorbic acid mediated strategy.
Glial soluble factors regulate the activity and expression of the neuronal glutamate transporter EAAC1: implication of cholesterol.
Metabotropic glutamate 5 receptor blockade alleviates akinesia by normalizing activity of selective basal-ganglia structures in parkinsonian rats.
Actualités
3 motivated and talented students successfully defended their thesis between February and July 2023.
5 motivated and talented students successfully defended their thesis between September 2022 and January 2023.
Lydia Kerkerian-Le Goff, Research Director at the CNRS and head of the Cellular Interactions, Neurodegeneration and Neuroplasticity team at the Marseille Institute of Developmental Biology (IBDM)
This study published in Cell Death & Disease, conducted by the team of L. Kerkerian-Le Goff provides the first evidence for a role of the stress-induced protein TP53INP1 in the maintenance of neuronal homeostasis in ageing and Parkinson’s disease-related stress conditions.
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