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34 Publication(s) en 2010 (1710 dans la base de données)
Boulanger J, Kervrann C, Bouthemy P, Elbau P, Sibarita JB, Salamero J. Patch-based nonlocal functional for denoising fluorescence microscopy image sequences. IEEE Trans Med Imaging. 2010 Feb;29(2):442-54.. 2010
IF : 4.004
Liens vers résumé
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| Collaboration nationale |
- Institut Curie, 26 rue d'Ulm, 75248 Paris Cedex 05, France. |
| Abstract |
We present a nonparametric regression method for denoising 3-D image sequences acquired via fluorescence microscopy. The proposed method exploits the redundancy of the 3-D+time information to improve the signal-to-noise ratio of images corrupted by Poisson-Gaussian noise. A variance stabilization transform is first applied to the image-data to remove the dependence between the mean and variance of intensity values. This preprocessing requires the knowledge of parameters related to the acquisition system, also estimated in our approach. In a second step, we propose an original statistical patch-based framework for noise reduction and preservation of space-time discontinuities. In our study, discontinuities are related to small moving spots with high velocity observed in fluorescence video-microscopy. The idea is to minimize an objective nonlocal energy functional involving spatio-temporal image patches. The minimizer has a simple form and is defined as the weighted average of input data taken in spatially-varying neighborhoods. The size of each neighborhood is optimized to improve the performance of the pointwise estimator. The performance of the algorithm (which requires no motion estimation) is then evaluated on both synthetic and real image sequences using qualitative and quantitative criteria. |
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Boulenguez P, Liabeuf S, Bos R, Bras H, Jean-Xavier C, Brocard C, Stil A, Darbon P, Cattaert D, Delpire E, Marsala M, Vinay L. Down-regulation of the potassium-chloride cotransporter KCC2 contributes to spasticity after spinal cord injury. Nat Med. 2010 Feb 28.. 2010
original article. IF : 27.553
Unité : Centre de Neurosciences Intégratives et Cognitives - Georges Di Scala
Liens vers résumé
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| Equipe |
Comportement et réseaux neuronaux - Daniel Cattaert |
| Axe de recherche |
Fonctions cognitives normales et pathologiques |
| Collaboration nationale |
- Laboratoire Plasticité et Physio-Pathologie de la Motricité (UMR6196), (CNRS) & Aix-Marseille Université, Marseille, France.
- Institut des Neurosciences Cellulaires et Intégratives, UPR3212 CNRS-Université de Strasbourg, Département Nociception et Douleur, Strasbourg, France |
| Collaboration européenne |
Institute of Neurobiology, Slovak Academy of Sciences, Kosice, Slovakia. |
| Collaboration internationale |
- Department of Anesthesiology, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
- Anesthesiology Research Laboratory, Department of Anesthesiology, University of California–San Diego, La Jolla, California, USA.
- Biozentrum, Department of Cell Biology, University of Basel, Basel, Switzerland and Friedrich Miescher Institute for Biomedical Research, Basel, Switzerland |
| Abstract |
Hyperexcitability of spinal reflexes and reduced synaptic inhibition are commonly associated with spasticity after spinal cord injury (SCI). In adults, the activation of gamma-aminobutyric acid(A) (GABA(A)) and glycine receptors inhibits neurons as a result of low intracellular chloride (Cl(-)) concentration, which is maintained by the potassium-chloride cotransporter KCC2 (encoded by Slc12a5). We show that KCC2 is downregulated after SCI in rats, particularly in motoneuron membranes, thereby depolarizing the Cl(-) equilibrium potential and reducing the strength of postsynaptic inhibition. Blocking KCC2 in intact rats reduces the rate-dependent depression (RDD) of the Hoffmann reflex, as is observed in spasticity. RDD is also decreased in KCC2-deficient mice and in intact rats after intrathecal brain-derived neurotrophic factor (BDNF) injection, which downregulates KCC2. The early decrease in KCC2 after SCI is prevented by sequestering BDNF at the time of SCI. Conversely, after SCI, BDNF upregulates KCC2 and restores RDD. Our results open new perspectives for the development of therapeutic strategies to alleviate spasticity. |
| Publication principale |
oui |
| Commentaire |
These authors contributed equally to this work. |
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Herry C, Ferraguti F, Singewald N, Letzkus J J, Ehrlich I, Lüthi A. Neuronal circuits of fear extinction. Eur J Neurosci. 2010 Feb; 31(4):p599-612. 2010
IF : 3.385
Unité : Physiopathologie de la plasticité neuronale - Pier Vincenzo Piazza
Liens vers résumé
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| Equipe |
Physiopathologie de la transmission et de la plasticité synaptique - Olivier Manzoni |
| Axe de recherche |
Synapse |
| Collaboration européenne |
- Department of Pharmacology, Innsbruck Medical University, 6020 Innsbruck, Austria
- Department of Pharmacology and Toxicology, Institute of Pharmacy and Center for - Molecular Biosciences Innsbruck, University of Innsbruck, Austria
- Friedrich Miescher Institute for Biomedical Research, CH-4058 Basel, Switzerland |
| Abstract |
Fear extinction is a form of inhibitory learning that allows for the adaptive control of conditioned fear responses. Although fear extinction is an active learning process that eventually leads to the formation of a consolidated extinction memory, it is a fragile behavioural state. Fear responses can recover spontaneously or subsequent to environmental influences, such as context changes or stress. Understanding the neuronal substrates of fear extinction is of tremendous clinical relevance, as extinction is the cornerstone of psychological therapy of several anxiety disorders and because the relapse of maladaptative fear and anxiety is a major clinical problem. Recent research has begun to shed light on the molecular and cellular processes underlying fear extinction. In particular, the acquisition, consolidation and expression of extinction memories are thought to be mediated by highly specific neuronal circuits embedded in a large-scale brain network including the amygdala, prefrontal cortex, hippocampus and brain stem. Moreover, recent findings indicate that the neuronal circuitry of extinction is developmentally regulated. Here, we review emerging concepts of the neuronal circuitry of fear extinction, and highlight novel findings suggesting that the fragile phenomenon of extinction can be converted into a permanent erasure of fear memories. Finally, we discuss how research on genetic animal models of impaired extinction can further our understanding of the molecular and genetic bases of human anxiety disorders. |
| Publication principale |
oui |
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Vendruscolo LF, Gueye AB, Darnaudéry M, Ahmed SH, Cador M. Sugar overconsumption during adolescence selectively alters motivation and reward function in adult rats.
PLoS One. 2010 Feb 19;5(2):e9296.. 2010
Unité : Mouvement - Adaptation - Cognition - Jean-René Cazalets ; Psychoneuroimmunologie, Nutrition et Génétique - Françoise Moos
Liens vers résumé
Lien vers Texte intégral |
| Equipe |
Neuropsychopharmacologie de l'addiction - Martine Cador ; Nutrition, Cytokines et troubles neuropsychiatriques - Sophie Layé |
| Axe de recherche |
Neuroinflammation |
| Collaboration nationale |
- Université Pierre et Marie Curie, France |
| Abstract |
BACKGROUND: There has been a dramatic escalation in sugar intake in the last few decades, most strikingly observed in the adolescent population. Sugar overconsumption has been associated with several adverse health consequences, including obesity and diabetes. Very little is known, however, about the impact of sugar overconsumption on mental health in general, and on reward-related behavioral disorders in particular. This study examined in rats the effects of unlimited access to sucrose during adolescence on the motivation for natural and pharmacological rewards in adulthood. METHODOLOGY/PRINCIPAL FINDINGS: Adolescent rats had free access to 5% sucrose or water from postnatal day 30 to 46. The control group had access to water only. In adulthood, rats were tested for self-administration of saccharin (sweet), maltodextrin (non-sweet), and cocaine (a potent drug of abuse) using fixed- and progressive-ratio schedules, and a concentration-response curve for each substance. Adult rats, exposed or not exposed to sucrose, were tested for saccharin self-administration later in life to verify the specificity of adolescence for the sugar effects. Sugar overconsumption during adolescence, but not during adulthood, reduced the subsequent motivation for saccharin and maltodextrin, but not cocaine. This selective decrease in motivation is more likely due to changes in brain reward processing than changes in gustatory perception. CONCLUSIONS/SIGNIFICANCE: Sugar overconsumption induces a developmental stage-specific chronic depression in reward processing that may contribute to an increase in the vulnerability to reward-related psychiatric disorders. |
| Commentaire |
Contributed equally |
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Collongues N, Marignier R, Zéphir H, Papeix C, Blanc F, Ritleng C, Tchikviladzé M, Outteryck O, Vukusic S, Fleury M, Fontaine B, Brassat D, Clanet M, Milh M, Pelletier J, Audoin B, Ruet A, Lebrun-Frenay C, Thouvenot E, Camu W, Debouverie M, Créange A, Moreau T, Labauge P, Castelnovo G, Edan G, Le Page E, Defer G, Barroso B, Heinzlef O, Gout O, Rodriguez D, Wiertlewski S, Laplaud D, Borgel F, Tourniaire P, Grimaud J, Brochet B, Vermersch P, Confavreux C, de Seze J. Neuromyelitis optica in France: A multicenter study of 125 patients.
Neurology. 2010 Mar 2;74(9):736-42.. 2010
original article. IF : 7.043
Liens vers résumé
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| Collaboration nationale |
- Department of Neurology, University Hospital of Strasbourg, 1, Place de l'Hôpital, 67091 Strasbourg, France
- University Hospital; Department of Neurology, Lyon
- University Hospital; Department of Neurology, Lille University Hospital
- Federation of Neurology, Pitié-Salpêtrière Hospital, Paris
- Department of Neurology (M.T.), Saint-Joseph Hospital, Paris; Department of Neurology Toulouse University Hospital
- Departments of Pediatrics and Neurology , Marseille University Hospital
- Department of Neurology, Nice University Hospital
- Department of Neurology, Montpellier University Hospital
- Department of Neurology, Nancy University Hospital
- Creteil Hospital
- Department of Neurology, Dijon University Hospital
- Department of Neurology, Nîmes University Hospital
- Department of Neurology, Rennes University Hospital
- Department of Neurology, Caen University Hospital
- Pau Hospital
Poissy Hospital
- Department of Neurology, Rothschild Foundation Hospital, Paris
- Department of Neurology, University Hospital of Trousseau, Paris
- Department of Neurology (S.W., D.L.), Nantes University Hospital
- the Department of Neurology, Grenoble University Hospital
- Avignon Hospital
- Chartres Hospital France. |
| Abstract |
BACKGROUND: There have been few epidemiologic studies on neuromyelitis optica (NMO) and none used the recent 2006 diagnostic criteria. Here we describe the clinical, laboratory, MRI, and disability course of NMO in a French cohort of 125 patients. METHODS: We performed an observational, retrospective, multicenter study. Data were collected from September 2007 through August 2008, corresponding to the endpoint of the study. We identified 125 patients fulfilling the 2006 NMO criteria. Selection was made using hospital files and a specific clinical questionnaire for NMO. RESULTS: Mean age at onset was 34.5 years (range 4-66) with a mean disease duration of 10 +/- 7.8 years at the endpoint. The patients were mainly (87%) Caucasian, with a female:male ratio of 3:1. In 90% of cases, the association of optic neuritis, longitudinal extensive myelitis, and a Paty-negative initial brain MRI was sufficient to fulfill the supportive criteria. Eighty-eight percent of patients were treated with immunosuppressive therapies. Median delay from onset to Expanded Disability Status Scale (EDSS) score 4 was 7 years; score 6, 10 years; and score 7, 21 years. The first episode of myelitis was immediately followed by an EDSS score >/=4 in 37.3% of cases, and a severe residual visual loss was observed in 22% of patients after the first episode of optic neuritis. Multivariate analysis did not reveal any predictors of a poor evolution other than a high number of MRI brain lesions at diagnosis, which were predictive of a residual visual acuity
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Deloire M, Ruet A, Hamel D, Bonnet M, Brochet B. Early cognitive impairment in multiple sclerosis predicts disability outcome several years later. Mult Scler. 2010 Mar 1. . 2010
original article. IF : 3.312
Unité : Neurobiologie des affections de la myéline - Klaus Petry ; Pôle de Neurosciences cliniques - Jean-Marc Orgogozo
Liens vers résumé
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| Equipe |
Neurobiologie des affections de la myéline - Klaus Petry ; Service de Neurologie - Bruno Brochet |
| Axe de recherche |
Neuroinflammation |
| Abstract |
Cognition is frequently impaired in the early stages of multiple sclerosis (MS). The predictive value of cognitive impairment on disability is unknown. The objective of this study was to correlate cognitive impairment and the progression of disability over 7 years. Forty-five patients, recruited after MS diagnosis, were followed for 7 years by yearly Expanded Disability Status Scale (EDSS) and Multiple Sclerosis Functional Composite (MSFC) evaluations and were classified as cognitively impaired (CI) or unimpaired (CU) according to neuropsychological testing at baseline. At baseline, 47.8% of patients were CI, with deficits in mainly memory and information processing speed (IPS). The baseline EDSS correlated significantly with one IPS test. The EDSS, but not the MSFC, deteriorated significantly over the 7 years in the whole group and the CI group, but not the CU group. A multivariate analysis showed correlations between the EDSS change over 5 and 7 years and two baseline tests evaluating IPS and verbal memory. The deterioration of the EDSS after 7 years was significantly correlated with verbal memory testing at baseline after adjustment for age and baseline EDSS. In conclusion, in this sample of MS patients early in the disease, the baseline IPS and verbal memory impairments predict the EDSS score 5 and 7 years later. |
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Veenstra JA. Neurohormones and neuropeptides encoded by the genome of Lottia gigantea, with reference to other mollusks and insects.
Gen Comp Endocrinol. 2010 Feb 18.. 2010
IF : 2.654
Unité : Centre de Neurosciences Intégratives et Cognitives - Georges Di Scala
Liens vers résumé
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| Equipe |
Neurogénétique comportementale - Wim Crusio |
| Abstract |
The Lottia gigantea genome was prospected for the presence of genes coding neuropeptides and neurohormones. Four genes code insulin-related peptides: two genes code molluscan insulin-like growth hormones, one gene an insulin very similar to vertebrate insulin, and the fourth a peptide related to drosophila insulin-like peptide 7. Four other genes encode the cysteine-knot proteins GPA2/GPB5 and bursicon/parabursicon. Another 37 genes code for precursors of the following neuropeptides: achatin, APGWamide, allatostatin C, allatotropin, buccalin (perhaps an allatostatin A homolog), cerebrin, CCAP, conopressin, elevenin (the predicted neuropeptide made by abdominal neuron 11 in Aplysia), egg laying hormone (two genes), enterin, feeding circuit activating neuropeptide (FCAP), FFamide, FMRFamide, GGNG, a GnRH-like peptide, the newly discovered LASGLVamide, LFRFamide, LFRYamide, LRNFVamide, luqin, lymnokinin, myomodulin (two genes), the newly discovered NKY, NPY, pedal peptide (three genes), PKYMDT, pleurin, PXFVamide, small cardioactive peptides, tachykinins (two genes) and WWamide (an allatostatin B homolog). One gene was found to encode FWISamide, while about 20 closely related genes were found to encode WWFamide. These small neuropeptides appear homologous to the NdWFamide, which contains d-Trp; these genes are similar to the Aplysia gene encoding NWFamide. Some of these peptides had not been previously identified from mollusks, such as the predicted hormones similar to Drosophila and vertebrate insulins, bursicon, the putative proctolin homolog PKYMDT and allatostatin C. Together with neuropeptides which are likely homologs of other insect neuropeptides, such as cerebrin and WWamide, this shows that despite significant differences the molluscan and arthropod neuropeptidomes are more similar than generally recognized. |
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Ibarra A, Feuillere N, Roller M, Lesburgere E, Beracochea D. Effects of chronic administration of Melissa officinalis L. extract on anxiety-like reactivity and on circadian and exploratory activities in mice.
Phytomedicine. 2010 Feb 17. 2010
original article. IF : 2.330
Unité : Centre de Neurosciences Intégratives et Cognitives - Georges Di Scala
Liens vers résumé
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| Equipe |
Mémoire, émotions, motivation et leurs interactions - Daniel Beracochea |
| Collaboration nationale |
- Naturex SA, Site d’Agroparc BP 1218, 84911 Avignon Cedex 9, France |
| Collaboration internationale |
- Naturex Inc, 375 Huyler St, South Hackensack, NJ 07606, USA |
| Abstract |
This study aimed to determine the effects of chronic (15 consecutive days of treatment) per os administration of Melissa officinalis L. extract (Cyracos((R)), Naturex) on anxiety-like reactivity in mice. As measured by HPLC, Cyracos((R)) contains significant amounts of rosmarinic acid and the triterpenoids oleanolic acid and ursolic acid, which inhibit gamma-aminobutyric acid transaminase (GABA-T) activity and increase GABA levels in the brain (Awad et al., 2007; Awad et al., 2009). Thus, we evaluated Cyracos((R)) use in independent groups of C57BL/6 mice with regard to anxiety-like reactivity in an elevated plus maze and an open field task. We found that Cyracos((R)) significantly reduced anxiety-like reactivity in the elevated plus maze dose-dependently, but no significant effect was observed in the open field task. Parallel experiments in independent groups of mice showed that the Cyracos((R)) dose at which it exerted anxiolytic-like effects in the elevated plus maze did not alter exploratory or circadian activities. Therefore, our results demonstrate that Cyracos((R)) has anxiolytic-like effects under moderate stress conditions and does not alter activity levels. |
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Berthet A, Bezard E. Dopamine receptors and L-dopa-induced dyskinesia.
Parkinsonism Relat Disord. 2009 Dec;15 Suppl 4:S8-12.. 2010
original article. IF : 1.907
Unité : Mouvement - Adaptation - Cognition - Jean-René Cazalets
Liens vers résumé
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| Equipe |
Physiopathologie des syndromes parkinsoniens - Erwan Bezard |
| Abstract |
In the majority of Parkinson's disease patients, chronic dopamine replacement therapy leads to involuntary aimless movements known as l-dopa-induced dyskinesia. While mechanisms involved in dyskinesia occurrence are still unclear, dopamine receptors undoubtedly have a central role in their pathophysiology. Here we review current knowledge and evidence for their involvement in dyskinesia genesis and manifestation. We propose that an anti-dyskinetic strategy should target the D1/D3 signalling cascade, as targeting D2 receptor signalling seems to inherently convey anti-therapeutic effects deleterious to patients. As more molecular tools are made available, we will better understand the role of each receptor and its associated signalling cascade in Parkinson's disease and L-dopa-induced dyskinesia, hopefully in a way amenable to patients. |
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Vital C, Lagueny A, Mercie P, Viallard JF, Delabrousse-Mayoux JP, Vital A. Usefulness of combined nerve and muscle biopsy in the diagnosis of amyloid neuropathy - a study of 6 new cases.
Clin Neuropathol. 2010 Mar-Apr;29(2):59-64.. 2010
IF : 1.200
Unité : Mouvement - Adaptation - Cognition - Jean-René Cazalets ; Pôle de Neurosciences cliniques - Jean-Marc Orgogozo
Liens vers résumé
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| Equipe |
Physiopathologie des syndromes parkinsoniens - Erwan Bezard ; Service de Neurologie - Bruno Brochet |
| Collaboration nationale |
- Bergerac Hospital, Bordeaux, France |
| Abstract |
Objective: Most cases of familial amyloid polyneuropathy are identified by molecular genetic analysis of the transthyretin (TTR) gene. However, it is not uncommon to find unexpected amyloid deposits marked by the anti-TTR serum in the endoneurium of aged patients. Light chain amyloid deposits may also be found in the endoneurium. During these past 5 years, we studied the muscle and nerve biopsies from 6 patients which revealed amyloid deposits. There were 2 patients with an idiopathic polyneuropathy and 4 with monoclonal gammopathy (MG). Methods: In each case, specimens from the superficial peroneal nerve and peroneus brevis muscle were taken by the same cutaneous incision. Results: Amyloid deposits were visible in the endoneurium of 2 cases and only on muscle specimens in 3 other cases, 1 with a MG and 2 with an idiopathic polyneuropathy. Amyloid deposits were strongly stained with the anti-TTR serum in the muscle specimens of the 2 idiopathic cases, mainly located in vessel walls. In one patient with polyneuropathy and MG, a small endoneurial amyloid deposit surprisingly revealed to be immunostained by the anti-TTR serum. In another case, a small amyloid deposit in close relationship with a macrophage was only visible in the endoneurium by electron microscopy. Comments: Amyloid deposits were only visible on muscle fragments in 3 cases and were strongly marked by the anti-TTR serum in 2 of them, indicating their familial origin. Combining muscle and nerve biopsy raises the number of cases with visible amyloid deposits. |
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