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86 Publication(s) en 2012 (2309 dans la base de données)
Bezard E, Pisani A, Berton O. Neuroscience disease models.
Neuroscience. 2012 Jun 1;211:1. 2012
original article. IF : 3.215
Liens vers résumé
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| Unité |
Institut des maladies neurodégénératives - Erwan Bezard |
| Equipe |
Physiopathologie des syndromes parkinsoniens - Erwan Bezard |
| Axe de recherche |
Motricité normale et pathologique ; Neuropsychopharmacologie et thérapeutiques des déficits - axe transversal |
| Abstract |
no abstract available |
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De Deurwaerdère P, Navailles S.
What can we expect from the serotonergic side of l-DOPA? Rev Neurol (Paris). 2012 May 2. 2012
original article. IF : 0.528
Liens vers résumé
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| Unité |
Institut des maladies neurodégénératives - Erwan Bezard |
| Equipe |
Monoamines, stimulation cérébrale profonde et maladie de Parkinson - Abdelhamid Benazzouz |
| Axe de recherche |
Motricité normale et pathologique |
| Abstract |
Parkinson's disease has long been associated with neurodegeneration of the dopaminergic neurons located in the substantia nigra. The metabolic precursor l-DOPA, administered exogenously to patients, has proven its superiority over other medications. Yet, its effectiveness is altered after long-term use by diverse motor and non-motor symptoms. Knowledge of its mechanism of action would be necessary to better apprehend the side effects, but do we really know where and how it works? The connexion between l-DOPA and the serotonergic system, after a sort of crusade lasting for more than 40 years, has been acknowledged recently. The purpose of this review, mainly based on preclinical data, is to present the pharmacological and biochemical evidence demonstrating that serotonergic neurons are mainly involved in the enhancement of dopamine transmission induced by l-DOPA. We are addressing thereafter the two main expectations coming from this mechanism that are fundamental and clinical. The fundamental part will focus on the conceptual framework imposed by such a mechanism, questioning notably the notion that the benefit of l-DOPA is associated with a restoration of dopamine levels in the caudate-putamen. The clinical part will discuss serotonergic strategies to ameliorate the benefit of l-DOPA treatment in line with past and current clinical trials. |
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Kim YH, Nonoguchi N, Paulus W, Brokinkel B, Keyvani K, Sure U, Wrede K, Mariani L, Giangaspero F, Tanaka Y, Nakazato Y, Vital A, Mittelbronn M, Perry A, Ohgaki H. Frequent BRAF Gain in Low-grade Diffuse Gliomas with 1p/19q Loss. Brain Pathol. 2012 May 9. 2012
original article. IF : 4.741
Liens vers résumé
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| Unité |
Institut des maladies neurodégénératives - Erwan Bezard |
| Equipe |
Physiopathologie des syndromes parkinsoniens - Erwan Bezard |
| Axe de recherche |
Motricité normale et pathologique ; Neuropsychopharmacologie et thérapeutiques des déficits - axe transversal |
| Collaboration nationale |
- Section of Molecular Pathology International Agency for Research on Cancer (IARC) 150 Cours Albert Thomas 69372 Lyon Cedex 08,
- International Agency for Research on Cancer, F-69372 Lyon, France
Institute of Neuropathology |
| Collaboration européenne |
- Department of Neurosurgery, University Hospital Munster, D-48149 Munster, Germany
Institute of Pathology and Neuropathology, Department of Neurosurgery, University Hospital Essen, D-45122 Essen, Germany
- Department of Radiological, Oncological and Anatomo-Pathological Sciences, University Sapienza, Rome, Italy and IRCCS Neuromed, Pozzilli, Italy
- Edinger Institute (Neurological Institute), Goethe University Hospital, D-60528 Frankfurt am Main, Germany |
| Collaboration internationale |
- University Hospital, Basel, CH-4031 and University Hospital, Bern, CH-3010, Switzerland
- Department of Pathology, Gunma University, Japan
- Department of Pathology, Division of Neuropathology, University of California, San Francisco (UCSF), San Francisco CA 94143 USA |
| Abstract |
Chromosomal 7q34 duplication and BRAF-KIAA1549 fusion is a characteristic genetic alteration in pilocytic astrocytomas. 7q34 gain appears to be common in diffuse astrocytomas, but its significance is unclear. We assessed BRAF gain and BRAF mutations in 123 low-grade diffuse gliomas, including 55 diffuse astrocytomas, 18 oligoastrocytomas and 50 oligodendrogliomas. Quantitative PCR revealed BRAF gain in 17/50 (34%) oligodendrogliomas, a significantly higher frequency than in diffuse astrocytomas (7/55; 13%; P=0.0112). BRAF gain was common in low-grade diffuse gliomas with 1p/19q loss (39%) and those lacking any of the genetic alterations analyzed (31%), but was rare in those with TP53 mutations (2%). Logistic regression analysis showed a significant positive association between 1p/19q loss and BRAF gain (P=0.0032) and a significant negative association between TP53 mutations and BRAF gain (P=0.0042). FISH analysis of 26 low-grade diffuse gliomas with BRAF gain additionally revealed BRAF-KIAA1549 fusion in one oligodendroglioma. Sequencing of cDNA in 17 low-grade diffuse gliomas showed BRAF-KIAA1549 fusion in another oligodendroglioma. A BRAF(V600E) mutation was also detected in one oligodendroglioma, and a BRAF(A598V) in one diffuse astrocytoma. These results suggest that low-grade diffuse gliomas with 1p/19q loss have frequent BRAF gains, and a small fraction of oligodendrogliomas may show BRAF-KIAA1549 fusion. |
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Nagaishi M, Kim YH, Mittelbronn M, Giangaspero F, Paulus W, Brokinkel B, Vital A, Tanaka Y, Nakazato Y, Legras-Lachuer C, Lachuer J, Ohgaki H. Amplification of the STOML3, FREM2, and LHFP Genes Is Associated with Mesenchymal Differentiation in Gliosarcoma.
Am J Pathol. 2012 May;180(5):1816-23. 2012
original article. IF : 5.224
Liens vers résumé
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| Unité |
Institut des maladies neurodégénératives - Erwan Bezard |
| Equipe |
Physiopathologie des syndromes parkinsoniens - Erwan Bezard |
| Axe de recherche |
Motricité normale et pathologique ; Neuropsychopharmacologie et thérapeutiques des déficits - axe transversal |
| Collaboration nationale |
- International Agency for Research on Cancer, Lyon, France
- ProfileXpert, University of Lyon, Lyon, France
- Centre de Recherche en Cancérologie de Lyon, UMR Inserm U1052 - CNRS U5286, Lyon, France |
| Collaboration européenne |
- Neurological Institute (Edinger Institute), Goethe University Hospital, Frankfurt, Frankfurt am Main, Germany
- Department of Radiological, Oncological, and Anatomo-Pathological Sciences, University Sapienza, Rome, Italy
- Institute of Neuropathology, University Hospital Muenster, Munster, Germany
- Department of Neurosurgery, University Hospital Muenster, Munster, Germany |
| Collaboration internationale |
- International Agency for Research on Cancer, Gunma University, Gunma, Japan
- Department of Pathology, Gunma University, Gunma, Japan |
| Abstract |
Gliosarcoma is a rare glioblastoma variant characterized by a biphasic tissue pattern with alternating areas that display either glial (glial fibrillary acidic protein-positive) or mesenchymal (reticulin-positive) differentiation. Previous analyses have shown identical genetic alterations in glial and mesenchymal tumor areas, suggesting that gliosarcomas are genetically monoclonal, and mesenchymal differentiation was considered to reflect the elevated genomic instability of glioblastomas. In the present study, we compared genome-wide chromosomal imbalances using array comparative genomic hybridization in glial and mesenchymal tumor areas of 13 gliosarcomas. The patterns of gain and loss were similar, except that the gain at 13q13.3-q14.1 (log(2) ratio >3.0), containing the STOML3, FREM2, and LHFP genes, which was restricted to the mesenchymal tumor area of a gliosarcoma. Further analyses of 64 cases of gliosarcoma using quantitative PCR showed amplification of the STOML3, FREM2, and LHFP genes in 14 (22%), 10 (16%), and 7 (11%) mesenchymal tumor areas, respectively, but not in glial tumor areas. Results of IHC analysis confirmed that overexpression of STOML3 and FREM2 was more extensive in mesenchymal than in glial tumor areas. These results suggest that the mesenchymal components in a small fraction of gliosarcomas may be derived from glial cells with additional genetic alterations. |
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Hill AA, Simmers J, Meyrand P, Massabuau JC. Modulation of network pacemaker neurons by oxygen at the anaerobic threshold. J Comp Physiol A Neuroethol Sens Neural Behav Physiol. 2012 Apr 22. 2012
IF : 2.000
Liens vers résumé
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| Unité |
Institut des maladies neurodégénératives - Erwan Bezard ; Institut de Neurosciences cognitives et intégratives d'Aquitaine - Jean-René Cazalets |
| Equipe |
Dynamique des réseaux neuronaux et vasculaires dans les processus mnésiques - Bruno Bontempi |
| Axe de recherche |
Synapse ; Motricité normale et pathologique ; Cognition normale et pathologique ; Neurobiologie du développement |
| Collaboration nationale |
Université de Bordeaux, EPOC, UMR 5805, 33120 Arcachon, France |
| Collaboration internationale |
New Jersey Institute of Technology, Rutgers University, Newark, NJ 07102, USA |
| Abstract |
Previous in vitro and in vivo studies showed that the frequency of rhythmic pyloric network activity in the lobster is modulated directly by oxygen partial pressure (PO(2)). We have extended these results by (1) increasing the period of exposure to low PO(2) and by (2) testing the sensitivity of the pyloric network to changes in PO(2) that are within the narrow range normally experienced by the lobster (1 to 6 kPa). We found that the pyloric network rhythm was indeed altered by changes in PO(2) within the range typically observed in vivo. Furthermore, a previous study showed that the lateral pyloric constrictor motor neuron (LP) contributes to the O(2) sensitivity of the pyloric network. Here, we expanded on this idea by testing the hypothesis that pyloric pacemaker neurons also contribute to pyloric O(2) sensitivity. A 2-h exposure to 1 kPa PO(2), which was twice the period used previously, decreased the frequency of an isolated group of pacemaker neurons, suggesting that changes in the rhythmogenic properties of these cells contribute to pyloric O(2) sensitivity during long-term near-anaerobic (anaerobic threshold, 0.7-1.2 kPa) conditions. |
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Brossaud J, Barat P, Fagour L, Corcuff JB. Cortisol assay in dried blood spots to reduce false positive rate in congenital adrenal hyperplasia screening.
Clin Chim Acta. 2012 Apr 25. 2012
original article. IF : 2.389
Liens vers résumé
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| Unité |
Laboratoire Nutrition et Neurobiologie intégrée - Sophie Layé |
| Equipe |
Nutrition, récepteurs nucléaires et vieillissement cérébral - Véronique Pallet |
| Axe de recherche |
Nutrition et cerveau ; Neuroinflammation |
| Collaboration nationale |
CHU de Bordeaux, Department of Nuclear Medicine, F-33604, Pessac, France
CHU de Bordeaux, Department of Pediatrics, F-33000, Bordeaux, France |
| Abstract |
BACKGROUND:
False positive tests (increased 17OH progesterone levels) for congenital adrenal hyperplasia are increasingly frequent due to better of premature neonates.
METHOD:
We added cortisol assay to 17OH progesterone assay on blotter papers to decrease the false positive rate.
RESULTS:
A cortisol concentration <85nmol/l (100% sensitivity) elicited a specificity of 43% for the diagnosis of congenital adrenal hyperplasia.
CONCLUSION:
As an alternative to more complex assays, a cortisol immunoassay can help neonate screening. |
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Barat P, Corcuff JB, Tauber M, Moisan MP. Associations of glucocorticoid receptor and corticosteroid-binding globulin gene polymorphisms on fat mass and fat mass distribution in prepubertal obese children. J Physiol Biochem. 2012 May 12. 2012
original article. IF : 1.357
Liens vers résumé
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| Unité |
Laboratoire Nutrition et Neurobiologie intégrée - Sophie Layé |
| Equipe |
Nutrition, récepteurs nucléaires et vieillissement cérébral - Véronique Pallet |
| Axe de recherche |
Nutrition et cerveau ; Neuroinflammation |
| Collaboration nationale |
Department of Pediatric Endocrinology, CHU Bordeaux, Bordeaux, France
Department of Nuclear Medicine, CHU Bordeaux,Bordeaux, France
Department of Pediatric Endocrinology, CHU Toulouse,Toulouse, France |
| Abstract |
Previous studies conducted in adult obese patients have shown that glucocorticoid receptor and corticosteroid-binding globulin gene polymorphisms influence cortisol-driven obesity and metabolic parameters. We investigated the impact of these polymorphisms in prepubertal obese children that were thoroughly examined for hypothalamic-pituitary-adrenal axis activity and for metabolic and obesity parameters. Obese children carrier of the allele G of the BclI polymorphism within glucocorticoid receptor gene tend to present a higher percentage of fat mass as well as a decreased cortisol suppression after low-dose dexamethasone as found in adult studies. Additionally, these allele G carriers show a strong correlation between truncal fat mass distribution and cortisol response to a standardized lunch, whereas this correlation is weak in allele C carriers. No differences were found for obesity or metabolic parameters between genotypes at the corticosteroid-binding globulin locus. However, allele 90 carriers present increased 24-h free urinary cortisol. Overall, this study provides new data showing the influence of glucocorticoid receptor and corticosteroid-binding globulin genes in obesity and/or cortisol action in prepubertal obese children. |
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Jacob W, Marsch R, Marsicano G, Lutz B, Wotjak CT. Cannabinoid CB1 receptor deficiency increases contextual fear memory under highly aversive conditions and long-term potentiation in vivo. Neurobiol Learn Mem. 2012 May 8. 2012
original article. IF : 3.701
Liens vers résumé
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| Unité |
Neurocentre Magendie - Physiopathologie de la plasticité neuronale - Pier Vincenzo Piazza |
| Equipe |
Endocannabinoïdes et neuroadaptation - Giovanni Marsicano |
| Axe de recherche |
Synapse ; Vulnérabilité et addictions ; Cognition normale et pathologique ; Nutrition et cerveau ; Neuropsychopharmacologie et thérapeutiques des déficits - axe transversal |
| Collaboration européenne |
Max Planck Institute of Psychiatry, Kraepelinstrasse 2, 80804 Munich, Germany |
| Abstract |
The cannabinoid receptor type 1 (CB1) is abundantly expressed in the central nervous system where it negatively controls the release of several neurotransmitters. CB1 activity plays a crucial role in learning and memory and in synaptic plasticity. In the present study, the role of CB1 was investigated in 3 different hippocampus-dependent memory tasks and in in vivo hippocampal synaptic plasticity in knockout (CB1-ko) and wildtype mice. There was no difference in short-term and long-term social and object recognition memory between CB1-ko and wildtype mice. In contrast, background contextual fear conditioning CB1-ko mice showed enhanced freezing levels in the conditioning context in and increased generalized contextual fear after a high-intensity conditioning foot shock of 1.5 mA, but not after 0.7 mA. In in vivo field potential recordings in the dentate gyrus, CB1-ko mice displayed a decreased paired-pulse facilitation of the populations spikes, suggesting an altered inhibitory synaptic drive onto hippocampal granule cells. Furthermore, CB1-ko mice displayed significantly higher levels of in vivo long-term potentiation (LTP) in the dentate gyrus. In conclusion, CB1 deficiency leads to enhanced contextual fear memory and altered synaptic plasticity in the hippocampus, supporting the key role of endocannabinoid signalling in learning and memory, in particular following highly aversive encounters. |
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Fassnacht M, Terzolo M, Allolio B, Baudin E, Haak H, Berruti A, Welin S, Schade-Brittinger C, Lacroix A, Jarzab B, Sorbye H, Torpy DJ, Stepan V, Schteingart DE, Arlt W, Kroiss M, Leboulleux S, Sperone P, Sundin A, Hermsen I, Hahner S, Willenberg HS, Tabarin A, Quinkler M, de la Fouchardière C, Schlumberger M, Mantero F, Weismann D, Beuschlein F, Gelderblom H, Wilmink H, Sender M, Edgerly M, Kenn W, Fojo T, Müller HH, Skogseid B; the FIRM-ACT Study Group. Combination Chemotherapy in Advanced Adrenocortical Carcinoma. N Engl J Med. 2012 May 2. 2012
Liens vers résumé
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| Unité |
Neurocentre Magendie - Physiopathologie de la plasticité neuronale - Pier Vincenzo Piazza |
| Equipe |
Physiopathologie de l'équilibre énergétique et obésité - Equipe AVENIR - Daniela Cota |
| Axe de recherche |
Neuropsychopharmacologie et thérapeutiques des déficits - axe transversal |
| Collaboration nationale |
the Department of Endocrinology, University of Bordeaux, Bordeaux, France
Centre Léon Bérard, Lyon, France
Service de Médecine Nucléaire et de Cancérologie Endocrinienne, Institut Gustave-Roussy, Villejuif, France |
| Collaboration européenne |
Comprehensive Cancer Center Mainfranken University of Würzburg, Würzburg, Germany
the Department of Clinical and Biological Sciences, Internal Medicine 1and Oncology University of Turin, Orbassano, Italy
the Department of Internal Medicine, Máxima Medical Center, Eindhoven, the Netherlands
the Department of Endocrine Oncology, University Hospital of Uppsala, Uppsala, Sweden
Coordinating Center for Clinical Trials, Philipps University, Marburg, Germany
the Department of Nuclear Medicine and Endocrine Oncology, Maria Sklodowska-Curie Memorial Cancer Center and Institute of Oncology, Gliwice, Poland
the Department of Internal Medicine, Elisabethinen Hospital, Graz, Austria
Centre for Endocrinology, Diabetes and Metabolism, School of Clinical and Experimental Medicine, Birmingham, UK
the Department of Radiology, Institute of Molecular Medicine and Surgery, Karolinska Institute, Stockholm
the Department of Endocrinology, Diabetes, and Rheumatology, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany
Clinical Endocrinology, Charité Campus Mitte, Charité University Medicine, Berlin Germany
the Department of Medical and Surgical Sciences, Endocrine Unit, Medical School, University of Padua, Padua, Italy
Medizinische Klinik und Poliklinik IV, Klinikum der Universität München, Munich, Germany
the Department of Clinical Oncology, Leiden University Medical Center, Leiden, the Netherlands
the Department of Medical Oncology, Academic Medical Center, Amsterdam
the Department of Oncology, Sahlgrenska University Hospital, Gothenburg, Sweden
Institute for Medical Informatics, Biometry, and Epidemiology, University of Munich, Munich, Germany
the Department of Medical Sciences, Uppsala University, Uppsala, Sweden
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| Collaboration internationale |
Medical Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD
the Department of Internal Medicine, University of Michigan, Ann Arbor
the Department of Medicine, Centre Hospitalier de l'Université de Montréal, Montreal
the Department of Oncology, Haukeland University Hospital, Bergen, Norway
Endocrine and Metabolic Unit, Royal Adelaide Hospital, Adelaide, SA, Australia |
| Abstract |
Background: Adrenocortical carcinoma is a rare cancer that has a poor response to cytotoxic treatment. Methods We randomly assigned 304 patients with advanced adrenocortical carcinoma to receive mitotane plus either a combination of etoposide (100 mg per square meter of body-surface area on days 2 to 4), doxorubicin (40 mg per square meter on day 1), and cisplatin (40 mg per square meter on days 3 and 4) (EDP) every 4 weeks or streptozocin (streptozotocin) (1 g on days 1 to 5 in cycle 1; 2 g on day 1 in subsequent cycles) every 3 weeks. Patients with disease progression received the alternative regimen as second-line therapy. The primary end point was overall survival. Results For first-line therapy, patients in the EDP-mitotane group had a significantly higher response rate than those in the streptozocin-mitotane group (23.2% vs. 9.2%, P<0.001) and longer median progression-free survival (5.0 months vs. 2.1 months; hazard ratio, 0.55; 95% confidence interval [CI], 0.43 to 0.69; P<0.001); there was no significant between-group difference in overall survival (14.8 months and 12.0 months, respectively; hazard ratio, 0.79; 95% CI, 0.61 to 1.02; P=0.07). Among the 185 patients who received the alternative regimen as second-line therapy, the median duration of progression-free survival was 5.6 months in the EDP-mitotane group and 2.2 months in the streptozocin-mitotane group. Patients who did not receive the alternative second-line therapy had better overall survival with first-line EDP plus mitotane (17.1 month) than with streptozocin plus mitotane (4.7 months). Rates of serious adverse events did not differ significantly between treatments. Conclusions Rates of response and progression-free survival were significantly better with EDP plus mitotane than with streptozocin plus mitotane as first-line therapy, with similar rates of toxic events, although there was no significant difference in overall survival. |
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Mikasova L, De Rossi P, Bouchet D, Georges F, Rogemond V, Didelot A, Meissirel C, Honnorat J, Groc L. Disrupted surface cross-talk between NMDA and Ephrin-B2 receptors in anti-NMDA encephalitis. Brain. 2012 May;135(Pt 5):1606-21. 2012
original article. IF : 9.232
Liens vers résumé
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| Unité |
Institut Interdisciplinaire de Neurosciences - Daniel Choquet |
| Equipe |
Développement et adaptation des circuits neuronaux - Laurent Groc |
| Axe de recherche |
Synapse ; Neurobiologie du développement |
| Collaboration nationale |
- Lyon Neuroscience Research Centre, INSERM U1028/CNRS UMR 5292, Université Claude Bernard Lyon 1 F-69372 Lyon, France
- Hospices Civils de Lyon, Hôpital Neurologique, Centre de Référence Maladie Rare ‘Syndromes neurologiques Paranéoplasiques’, F-69677 Bron, France |
| Abstract |
Autoimmune synaptic encephalitides are recently described human brain diseases leading to psychiatric and neurological syndromes through inappropriate brain-autoantibody interactions. The most frequent synaptic autoimmune encephalitis is associated with autoantibodies against extracellular domains of the glutamatergic N-methyl-d-aspartate receptor, with patients developing psychotic and neurological symptoms in an autoantibody titre-dependent manner. Although N-methyl-d-aspartate receptors are the primary target of these antibodies, the cellular and molecular pathway(s) that rapidly lead to N-methyl-d-aspartate receptor dysfunction remain poorly understood. In this report, we used a unique combination of high-resolution nanoparticle and bulk live imaging approaches to demonstrate that anti-N-methyl-d-aspartate receptor autoantibodies from patients with encephalitis strongly alter, in a time-dependent manner, the surface content and trafficking of GluN2-NMDA receptor subtypes. Autoantibodies laterally displaced surface GluN2A-NMDA receptors out of synapses and completely blocked synaptic plasticity. This loss of extrasynaptic and synaptic N-methyl-d-aspartate receptor is prevented both in vitro and in vivo, by the activation of EPHB2 receptors. Indeed, the anti-N-methyl-d-aspartate receptor autoantibodies weaken the interaction between the extracellular domains of the N-methyl-d-aspartate and Ephrin-B2 receptors. Together, we demonstrate that the anti-N-methyl-d-aspartate receptor autoantibodies from patients with encephalitis alter the dynamic retention of synaptic N-methyl-d-aspartate receptor through extracellular domain-dependent mechanism(s), shedding new light on the pathology of the neurological and psychiatric disorders observed in these patients and opening possible new therapeutic strategies. |
| Publication principale |
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