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Accueil du site > Equipes de recherche > Equipe CMO (N.Ravel, N.Buonviso) > Annuaire > Pages personnelles > Corine AMAT-PION


par Philippe Litaudon - 14 mai 2014


  • Fourcaud-Trocmé N, Briffaud V, Thévenet M, Buonviso N, Amat C. In vivo beta and gamma subthreshold oscillations in rat mitral cells: origin and gating by respiratory dynamics. Journal of Neurophysiology.:jn.00053.2017.
    Résumé : In mammals, olfactory bulb (OB) dynamics are paced by slow and fast oscillatory rhythms at multiple levels: local field potential, spike discharge, and/or membrane potential oscillations. Interactions between these levels have been well studied for the slow rhythm linked to animal respiration. However, less is known regarding rhythms in the fast beta (10-35Hz) and gamma (35-100Hz) frequency ranges, particularly at the membrane potential level. Using a combination of intracellular and extracellular recordings in the OB of freely breathing rats, we show that beta and gamma subthreshold oscillations (STO) coexist intracellularly and are related to extracellular LFP oscillations in the same frequency range. However, they are differentially affected by changes in cell excitability and by odor stimulation. This leads us to suggest that beta and gamma STOs may rely on distinct mechanisms: gamma STOs would mainly depend on mitral cell intrinsic resonance while beta STOs could be mainly driven by synaptic activity. In a second part, we found that STO occurrence and timing are constrained by the influence of the slow respiratory rhythm on mitral/tufted cells. First, respiratory-driven excitation seems to favor gamma STOs while respiratory-driven inhibition favors beta STOs. Second, the respiratory rhythm is needed at the subthreshold level in order to lock gamma and beta STOs in similar phases as their LFP counterparts and to favor the correlation between STO frequency and spike discharge. Overall, this study helps to understand how the interaction between slow and fast rhythms at all levels of OB dynamics shapes its functional output.
    Mots-clés : freely breathing anesthetized rat, mammalian olfactory bulb, odor stimulation, respiratory slow rhythm.


  • Laurent C, Burnouf S, Ferry B, et al. A2A adenosine receptor deletion is protective in a mouse model of Tauopathy. Molecular Psychiatry. 21(1):97-107.
    Résumé : Consumption of caffeine, a non-selective adenosine A2A receptor (A2AR) antagonist, reduces the risk of developing Alzheimer's disease (AD) in humans and mitigates both amyloid and Tau burden in transgenic mouse models. However, the impact of selective A2AR blockade on the progressive development of AD-related lesions and associated memory impairments has not been investigated. In the present study, we removed the gene encoding A2AR from THY-Tau22 mice and analysed the subsequent effects on both pathological (Tau phosphorylation and aggregation, neuro-inflammation) and functional impairments (spatial learning and memory, hippocampal plasticity, neurotransmitter profile). We found that deleting A2ARs protect from Tau pathology-induced deficits in terms of spatial memory and hippocampal long-term depression. These effects were concomitant with a normalization of the hippocampal glutamate/gamma-amino butyric acid ratio, together with a global reduction in neuro-inflammatory markers and a decrease in Tau hyperphosphorylation. Additionally, oral therapy using a specific A2AR antagonist (MSX-3) significantly improved memory and reduced Tau hyperphosphorylation in THY-Tau22 mice. By showing that A2AR genetic or pharmacological blockade improves the pathological phenotype in a Tau transgenic mouse model, the present data highlight A2A receptors as important molecular targets to consider against AD and Tauopathies.


  • Luppi P-H, Clément O, Sapin E, et al. The neuronal network responsible for paradoxical sleep and its dysfunctions causing narcolepsy and rapid eye movement (REM) behavior disorder. Sleep Medicine Reviews. 15(3):153-163.
    Résumé : Rapid eye movement (REM) sleep behavior disorder (RBD) is a parasomnia characterized by the loss of muscle atonia during paradoxical (REM) sleep (PS). Conversely, cataplexy, one of the key symptoms of narcolepsy, is a striking sudden episode of muscle weakness triggered by emotions during wakefulness, and comparable to REM sleep atonia. The neuronal dysfunctions responsible for RBD and cataplexy are not known. In the present review, we present the most recent results on the neuronal network responsible for PS. Based on these results, we propose an updated integrated model of the mechanisms responsible for PS and explore different hypotheses explaining RBD and cataplexy. We propose that RBD is due to a specific degeneration of a sub-population of PS-on glutamatergic neurons specifically responsible of muscle atonia, localized in the caudal pontine sublaterodorsal tegmental nucleus (SLD). Another possibility is the occurrence in RBD patients of a specific lesion of the glycinergic/GABAergic pre-motoneurons localized in the medullary ventral gigantocellular reticular nucleus. Conversely, cataplexy in narcoleptics would be due to the activation during waking of the caudal PS-on SLD neurons responsible for muscle atonia. A phasic glutamatergic excitatory pathway from the central amygdala to the SLD PS-on neurons activated during emotion would induce such activation. In normal conditions, the glutamate excitation would be blocked by the simultaneous excitation by the hypocretins of the PS-off GABAergic neurons localized in the ventrolateral periaqueductal gray and the adjacent deep mesencephalic reticular nucleus, gating the activation of the PS-on SLD neurons.
    Mots-clés : Amygdala, Animals, Brain, Brain Mapping, Cataplexy, Emotions, gamma-Aminobutyric Acid, Glutamine, Glycine, Humans, Hypothalamus, Medulla Oblongata, Motor Neurons, Muscle Tonus, Narcolepsy, Nerve Net, Neurodegenerative Diseases, Neurons, Parkinson Disease, Pedunculopontine Tegmental Nucleus, Pons, REM Sleep Behavior Disorder, Sleep, REM, Wakefulness.