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3. Phenotypical Screening on Neuronal Plasticity in Hippocampal-Prefrontal Cortex Connectivity Reveals an Antipsychotic with a Novel Profile

Author

Spedding, Michael, primary, Sebban, Claude, additional, Jay, Thérèse M., additional, Rocher, Cyril, additional, Tesolin-Decros, Brigitte, additional, Chazot, Paul, additional, Schenker, Esther, additional, Szénási, Gabor, additional, Lévay, György I., additional, Megyeri, Katalin, additional, Barkóczy, Jozsef, additional, Hársing, Laszlo G., additional, Thomson, Ian, additional, Cunningham, Mark O., additional, Whittington, Miles A., additional, Etherington, Lori-An, additional, Lambert, Jeremy J., additional, Antoni, Ferenc A., additional, and Gacsályi, Istvan, additional

Published
2022
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5. Systematic review of guidelines for internal validity in the design, conduct and analysis of preclinical biomedical experiments involving laboratory animals

Author

Vollert, Jan, Schenker, Esther, Macleod, Malcolm, Bespalov, Anton, Wuerbel, Hanno, Michel, Martin, Dirnagl, Ulrich, Potschka, Heidrun, Waldron, Ann-Marie, Wever, Kimberley, Steckler, Thomas, Van De Casteele, Tom, Altevogt, Bruce, Sil, Annesha, and Rice, Andrew S C

Subjects
630 Agriculture, 590 Animals (Zoology)
Abstract

Over the last two decades, awareness of the negative repercussions of flaws in the planning, conduct and reporting of preclinical research involving experimental animals has been growing. Several initiatives have set out to increase transparency and internal validity of preclinical studies, mostly publishing expert consensus and experience. While many of the points raised in these various guidelines are identical or similar, they differ in detail and rigour. Most of them focus on reporting, only few of them cover the planning and conduct of studies. The aim of this systematic review is to identify existing experimental design, conduct, analysis and reporting guidelines relating to preclinical animal research. A systematic search in PubMed, Embase and Web of Science retrieved 13 863 unique results. After screening these on title and abstract, 613 papers entered the full-text assessment stage, from which 60 papers were retained. From these, we extracted unique 58 recommendations on the planning, conduct and reporting of preclinical animal studies. Sample size calculations, adequate statistical methods, concealed and randomised allocation of animals to treatment, blinded outcome assessment and recording of animal flow through the experiment were recommended in more than half of the publications. While we consider these recommendations to be valuable, there is a striking lack of experimental evidence on their importance and relative effect on experiments and effect sizes

Published
2020
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6. Pharmacological Transdifferentiation of Human Nasal Olfactory Stem Cells into Dopaminergic Neurons

Author

Chabrat, Audrey, primary, Lacassagne, Emmanuelle, additional, Billiras, Rodolphe, additional, Landron, Sophie, additional, Pontisso-Mahout, Amélie, additional, Darville, Hélène, additional, Dupront, Alain, additional, Coge, Francis, additional, Schenker, Esther, additional, Piwnica, David, additional, Nivet, Emmanuel, additional, Féron, François, additional, and Mannoury la Cour, Clotilde, additional

Published
2019
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7. Reproducibility via coordinated standardization : a multi-center study in a S hank2 genetic rat model for Autism Spectrum Disorders

Author

Arroyo-Araujo, María, Graf, Radka, Maco, Martine, van Dam, Elsbeth, Schenker, Esther, Drinkenburg, Wilhelmus, Koopmans, Bastijn, de Boer, Sietse F., Cullum-Doyle, Michaela, Noldus, Lucas P.J.J., Loos, Maarten, van Dommelen, Wil, Spooren, Will, Biemans, Barbara, Buhl, Derek L., Kas, Martien J., Arroyo-Araujo, María, Graf, Radka, Maco, Martine, van Dam, Elsbeth, Schenker, Esther, Drinkenburg, Wilhelmus, Koopmans, Bastijn, de Boer, Sietse F., Cullum-Doyle, Michaela, Noldus, Lucas P.J.J., Loos, Maarten, van Dommelen, Wil, Spooren, Will, Biemans, Barbara, Buhl, Derek L., and Kas, Martien J.

Published
2019

8. Reproducibility via coordinated standardization: a multi-center study in a S hank2 genetic rat model for Autism Spectrum Disorders

Author

Translational Neuroscience, Arroyo-Araujo, María, Graf, Radka, Maco, Martine, van Dam, Elsbeth, Schenker, Esther, Drinkenburg, Wilhelmus, Koopmans, Bastijn, de Boer, Sietse F., Cullum-Doyle, Michaela, Noldus, Lucas P.J.J., Loos, Maarten, van Dommelen, Wil, Spooren, Will, Biemans, Barbara, Buhl, Derek L., Kas, Martien J., Translational Neuroscience, Arroyo-Araujo, María, Graf, Radka, Maco, Martine, van Dam, Elsbeth, Schenker, Esther, Drinkenburg, Wilhelmus, Koopmans, Bastijn, de Boer, Sietse F., Cullum-Doyle, Michaela, Noldus, Lucas P.J.J., Loos, Maarten, van Dommelen, Wil, Spooren, Will, Biemans, Barbara, Buhl, Derek L., and Kas, Martien J.

Published
2019

9. Acute Stress Affects the Expression of Hippocampal Mu Oscillations in an Age-Dependent Manner

Author

Takillah, Samir, Naudé, Jérémie, Didienne, Steve, Sebban, Claude, Decros, Brigitte, Schenker, Esther, Spedding, Michael, Mourot, Alexandre, Mariani, Jean, Faure, Philippe, Développement, Réparation et Vieillissement Cérébral ( DRVC ), Adaptation Biologique et Vieillissement = Biological Adaptation and Ageing ( B2A ), Centre National de la Recherche Scientifique ( CNRS ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Université Pierre et Marie Curie - Paris 6 ( UPMC ) -Centre National de la Recherche Scientifique ( CNRS ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Université Pierre et Marie Curie - Paris 6 ( UPMC ), Département Hospitalo-Universitaire Fight Ageing and STress ( DHU FAST ), Université Pierre et Marie Curie - Paris 6 ( UPMC ), Institut de Recherche Biomédicale des Armée [Brétigny/Orge] ( IRBA ), Sommeil-Vigilance-Fatigue et Santé Publique ( VIFASOM - EA 7330 ), Université Paris Descartes - Paris 5 ( UPD5 ), Neurophysiologie et comportements = Neurophysiology and Behavior ( NPS-06 ), Neuroscience Paris Seine ( NPS ), Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Université Pierre et Marie Curie - Paris 6 ( UPMC ) -Centre National de la Recherche Scientifique ( CNRS ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Université Pierre et Marie Curie - Paris 6 ( UPMC ) -Centre National de la Recherche Scientifique ( CNRS ), Centre National de la Recherche Scientifique ( CNRS ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Université Pierre et Marie Curie - Paris 6 ( UPMC ), Institut de Recherches Servier, Spedding Research solutions SARL, HAL UPMC, Gestionnaire, Développement, Réparation et Vieillissement Cérébral (DRVC), Adaptation Biologique et Vieillissement = Biological Adaptation and Ageing (B2A), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Département Hospitalo-Universitaire Fight Ageing and STress (DHU FAST ), Université Pierre et Marie Curie - Paris 6 (UPMC), Institut de Recherche Biomédicale des Armée [Brétigny/Orge] (IRBA), Sommeil-Vigilance-Fatigue et Santé Publique (VIFASOM - EA 7330), Université Paris Descartes - Paris 5 (UPD5)-Institut de Recherche Biomédicale des Armées (IRBA), Neurophysiologie et comportements = Neurophysiology and Behavior (NPS-06), Neuroscience Paris Seine (NPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Institut de Recherche Biomédicale des Armées (IRBA)-Université Paris Descartes - Paris 5 (UPD5), Neurosciences Paris Seine (NPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut de Biologie Paris Seine (IBPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut de Biologie Paris Seine (IBPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS), Université Paris Descartes - Paris 5 (UPD5)-Institut de Recherche Biomédicale des Armées [Brétigny-sur-Orge] (IRBA), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), and Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)

Subjects
stress, hippocampus, [ SDV.NEU ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], aging, synchronized oscillation, Mu-rhythm, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], [SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], Neuroscience
Abstract

International audience; Anxiolytic drugs are widely used in the elderly, a population particularly sensitive to stress. Stress, aging and anxiolytics all affect low-frequency oscillations in the hippocampus and prefrontal cortex (PFC) independently, but the interactions between these factors remain unclear. Here, we compared the effects of stress (elevated platform, EP) and anxiolytics (diazepam, DZP) on extracellular field potentials (EFP) in the PFC, parietal cortex and hippocampus (dorsal and ventral parts) of adult (8 months) and aged (18 months) Wistar rats. A potential source of confusion in the experimental studies in rodents comes from locomotion-related theta (6–12 Hz) oscillations, which may overshadow the direct effects of anxiety on low-frequency and especially on the high-amplitude oscillations in the Mu range (7–12 Hz), related to arousal. Animals were restrained to avoid any confound and isolate the direct effects of stress from theta oscillations related to stress-induced locomotion. We identified transient, high-amplitude oscillations in the 7–12 Hz range (" Mu-bursts ") in the PFC, parietal cortex and only in the dorsal part of hippocampus. At rest, aged rats displayed more Mu-bursts than adults. Stress acted differently on Mu-bursts depending on age: it increases vs. decreases burst, in adult and aged animals, respectively. In contrast DZP (1 mg/kg) acted the same way in stressed adult and age animal: it decreased the occurrence of Mu-bursts, as well as their co-occurrence. This is consistent with DZP acting as a positive allosteric modulator of GABA A receptors, which globally potentiates inhibition and has anxiolytic effects. Overall, the effect of benzodiazepines on stressed animals was to restore Mu burst activity in adults but to strongly diminish them in aged rats. This work suggests Mu-bursts as a neural marker to study the impact of stress and DZP on age.

Published
2017
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10. Clozapine counteracts a ketamine-induced depression of hippocampal-prefrontal neuroplasticity and alters signaling pathway phosphorylation

Author

Rame, Marion, Caudal, Dorian, Schenker, Esther, Svenningsson, Per, Spedding, Michael, Jay, Thérèse M., and Godsil, Bill P.

Subjects
Male, Physiology, Blotting, Western, lcsh:Medicine, Prefrontal Cortex, Nerve Tissue Proteins, Biochemistry, Hippocampus, Rats, Sprague-Dawley, Drug Therapy, Mental Health and Psychiatry, Medicine and Health Sciences, Animals, Post-Translational Modification, Phosphorylation, lcsh:Science, Clozapine, Neuronal Plasticity, Pharmaceutics, Mood Disorders, Depression, lcsh:R, Biology and Life Sciences, Proteins, Brain, Rats, Electrophysiology, nervous system, Cellular Neuroscience, Schizophrenia, lcsh:Q, Ketamine, Anatomy, Research Article, Neuroscience, Signal Transduction
Abstract

Single sub-anesthetic doses of ketamine can exacerbate the symptoms of patients diagnosed with schizophrenia, yet similar ketamine treatments rapidly reduce depressive symptoms in major depression. Acute doses of the atypical antipsychotic drug clozapine have also been shown to counteract ketamine-induced psychotic effects. In the interest of understanding whether these drug effects could be modeled with alterations in neuroplasticity, we examined the impact of acutely-administered ketamine and clozapine on in vivo long-term potentiation (LTP) in the rat's hippocampus-to-prefrontal cortex (H-PFC) pathway. We found that a low dose of ketamine depressed H-PFC LTP, whereas animals that were co-administrated the two drugs displayed LTP that was similar to a saline-treated control. To address which signaling molecules might mediate such effects, we also examined phosphorylation and total protein levels of GSK3β, GluA1, TrkB, ERK, and mTOR in prefrontal and hippocampal sub-regions. Among the statistically significant effects that were detected (a) both ketamine and clozapine increased the phosphorylation of Ser9-GSK3β throughout the prefrontal cortex and of Ser2481-mTOR in the dorsal hippocampus (DH), (b) clozapine increased the phosphorylation of Ser831-GluA1 throughout the prefrontal cortex and of Ser845-GluA1 in the ventral hippocampus, (c) ketamine treatment increased the phosphorylation of Thr202/Tyr204-ERK in the medial PFC (mPFC), and (d) clozapine treatment was associated with decreases in the phosphorylation of Tyr705-TrkB in the DH and of Try816-TrkB in the mPFC. Further analyses involving phosphorylation effect sizes also suggested Ser831-GluA1 in the PFC displayed the highest degree of clozapine-responsivity relative to ketamine. These results provide evidence for how ketamine and clozapine treatments affect neuroplasticity and signaling pathways in the stress-sensitive H-PFC network. They also demonstrate the potential relevance of H-PFC pathway neuroplasticity for modeling ketamine-clozapine interactions in regards to psychosis.

Published
2017

11. Effects of acute administration of donepezil or memantine on sleep-deprivation-induced spatial memory deficit in young and aged non-human primate grey mouse lemurs (Microcebus murinus)

Author

Rahman, Anisur, Lamberty, Yves, Schenker, Esther, Cella, Massimo, Languille, Solène, Bordet, Régis, Richardson, Jill, Pifferi, Fabien, Aujard, Fabienne, Mécanismes Adaptatifs et Evolution (MECADEV), Muséum national d'Histoire naturelle (MNHN)-Centre National de la Recherche Scientifique (CNRS), UCB Pharma S.A.[Braine-l'Alleud], Institut de Recherches SERVIER (IRS), Chiesi Farmaceutici, Université Lille Nord de France (COMUE), Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), GlaxoSmithKline, Glaxo Smith Kline, This work was financially supported as part of the Pharma-Cog consortium by the European Community’s Seventh Framework Programme for the Innovative Medicine Initiative under Grant Agreement no. 115009., UCB Pharma [Brussels], and Aujard, Fabienne

Subjects
Male, Aging, MESH: Aging/drug effects, lcsh:Medicine, Cognition, Learning and Memory, Piperidines, Medicine and Health Sciences, MESH: Animals, Donepezil, lcsh:Science, Spatial Memory, Animal Management, Cognitive Impairment, Mammals, Cognitive Neurology, MESH: Sleep Deprivation/physiopathology, Neurodegenerative Diseases, Agriculture, Animal Models, MESH: Alzheimer Disease/physiopathology, Neurology, Experimental Organism Systems, Indans, Vertebrates, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], MESH: Cheirogaleidae, Cheirogaleidae, MESH: Sleep Deprivation/complications, Research Article, MESH: Memory Disorders/etiology, Primates, Lemurs, MESH: Sleep Deprivation/drug therapy, Cognitive Neuroscience, Prosimians, Mouse Models, Research and Analysis Methods, Model Organisms, MESH: Spatial Memory/drug effects, Alzheimer Disease, Memantine, Memory, Mental Health and Psychiatry, Animals, MESH: Alzheimer Disease/drug therapy, [SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], MESH: Alzheimer Disease/complications, MESH: Donepezil, Memory Disorders, Animal Performance, MESH: Memory Disorders/physiopathology, lcsh:R, MESH: Memantine/pharmacology, Organisms, Biology and Life Sciences, Animal Cognition, MESH: Male, MESH: Memory Disorders/drug therapy, Disease Models, Animal, MESH: Piperidines/pharmacology, Amniotes, Sleep Deprivation, Cognitive Science, lcsh:Q, MESH: Indans/pharmacology, Dementia, MESH: Disease Models, Animal, Zoology, Neuroscience
Abstract

International audience; The development of novel therapeutics to prevent cognitive decline of Alzheimer's disease (AD) is facing paramount difficulties since the translational efficacy of rodent models did not resulted in better clinical results. Currently approved treatments, including the acetylcholinesterase inhibitor donepezil (DON) and the N-methyl-D-aspartate antagonist memantine (MEM) provide marginal therapeutic benefits to AD patients. There is an urgent need to develop a predictive animal model that is phylogenetically proximal to humans to achieve better translation. The non-human primate grey mouse lemur (Microcebus murinus) is increasingly used in aging research, but there is no published results related to the impact of known pharmacological treatments on age-related cognitive impairment observed in this primate. In the present study we investigated the effects of DON and MEM on sleep-deprivation (SD)-induced memory impairment in young and aged male mouse lemurs. In particular, spatial memory impairment was evaluated using a circular platform task after 8 h of total SD. Acute single doses of DON or MEM (0.1 and 1mg/kg) or vehicle were administered intraperitoneally 3 h before the cognitive task during the SD procedure. Results indicated that both doses of DON were able to prevent the SD-induced deficits in retrieval of spatial memory as compared to vehicle-treated animals, both in young and aged animals Likewise, MEM show a similar profile at 1 mg/kg but not at 0.1mg/kg. Taken together, these results indicate that two widely used drugs for mitigating cognitive deficits in AD were partially effective in sleep deprived mouse lemurs, which further support the translational potential of this animal model. Our findings demonstrate the utility of this primate model for further testing cognitive enhancing drugs in development for AD or other neuropsychiatric conditions.

Published
2017
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12. Deficits of psychomotor and mnesic functions across aging in mouse lemur primates

Author

Languille, Solène, Liévin-Bazin, Agatha, Picq, Jean-Luc, Louis, Caroline, Dix, Sophie, De Barry, Jean, Blin, Olivier, Richardson, Jill, Bordet, Régis, Schenker, Esther, Djelti, Fathia, Aujard, Fabienne, Mécanismes adaptatifs : des organismes aux communautés, Muséum national d'Histoire naturelle (MNHN)-Centre National de la Recherche Scientifique (CNRS), Laboratoire de Psychopathologie et Neuropsychologie (LPN), Université Paris 8 Vincennes-Saint-Denis (UP8), Institut de Recherches Servier, Eli Lilly, Erl Wood Manor, INCI UPR3212 et Innovative Health Diagnostics, Centre National de la Recherche Scientifique (CNRS), Aix Marseille Université (AMU), Centre investigation clinique - Unité de pharmacologie clinique et d'évaluations thérapeutiques (CIC-UPCET), Assistance Publique - Hôpitaux de Marseille (APHM), GlaxoSmithKline, R&D China U.K. Group Stevenage, Pharmacologie de la mort neuronale et de la plasticité cérébrale, IFR114-Université de Lille, Droit et Santé, Mécanismes adaptatifs : des organismes aux communautés (MECADEV), Institut des Neurosciences Cellulaires et Intégratives (INCI), and Université de Strasbourg (UNISTRA)-Centre National de la Recherche Scientifique (CNRS)

Subjects
Behavioral Neuroscience, Neuropsychology and Physiological Psychology, Cognitive Neuroscience, [SCCO.NEUR]Cognitive science/Neuroscience, Original Research Article, spatial memory, recognition memory, anxiety, psychomotor, working memory, Neuroscience
Abstract

International audience; Owing to a similar cerebral neuro-anatomy, non-human primates are viewed as the most valid models for understanding cognitive deficits. This study evaluated psychomotor and mnesic functions of 41 young to old mouse lemurs (Microcebus murinus). Psychomotor capacities and anxiety-related behaviors decreased abruptly from middle to late adulthood. However, mnesic functions were not affected in the same way with increasing age. While results of the spontaneous alternation task point to a progressive and widespread age-related decline of spatial working memory, both spatial reference and novel object recognition (NOR) memory tasks did not reveal any tendency due to large inter-individual variability in the middle-aged and old animals. Indeed, some of the aged animals performed as well as younger ones, whereas some others had bad performances in the Barnes maze and in the object recognition test. Hierarchical cluster analysis revealed that declarative-like memory was strongly impaired only in 7 out of 25 middle-aged/old animals. These results suggest that this analysis allows to distinguish elder populations of good and bad performers in this non-human primate model and to closely compare this to human aging.

Published
2015
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14. In search of the mechanisms of ketamine’s antidepressant effects: How robust is the evidence behind the mTor activation hypothesis

Author

Popp, Susanna, primary, Behl, Berthold, additional, Joshi, Jaya Julie, additional, Lanz, Thomas A., additional, Spedding, Michael, additional, Schenker, Esther, additional, Jay, Therese M, additional, Svenningsson, Per, additional, Caudal, Dorian, additional, Cunningham, Jacob I., additional, Deaver, Daniel, additional, and Bespalov, Anton, additional

Published
2016
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15. HDAC6 as a target for neurodegenerative diseases: what makes it different from the other HDACs?

Author

Simoes Avello, Claudia, Zwick, Vincent, Nurisso, Alessandra, Schenker, Esther, Carrupt, Pierre-Alain, and Cuendet, Muriel

Subjects
ddc:615, Neurodegenerative diseases, Histone deacetylase, HDAC6
Abstract

Histone deacetylase (HDAC) inhibitors have been demonstrated to be beneficial in animal models of neurodegenerative diseases. Such results were mainly associated with the epigenetic modulation caused by HDACs, especially those from class I, via chromatin deacetylation. However, other mechanisms may contribute to the neuroprotective effect of HDAC inhibitors, since each HDAC may present distinct specific functions within the neurodegenerative cascades. Such an example is HDAC6 for which the role in neurodegeneration has been partially elucidated so far. The strategy to be adopted in promising therapeutics targeting HDAC6 is still controversial. Specific inhibitors exert neuroprotection by increasing the acetylation levels of α-tubulin with subsequent improvement of the axonal transport, which is usually impaired in neurodegenerative disorders. On the other hand, an induction of HDAC6 would theoretically contribute to the degradation of protein aggregates which characterize various neurodegenerative disorders, including Alzheimer's, Parkinson's and Hutington's diseases. This review describes the specific role of HDAC6 compared to the other HDACs in the context of neurodegeneration, by collecting in silico, in vitro and in vivo results regarding the inhibition and/or knockdown of HDAC6 and other HDACs. Moreover, structure, function, subcellular localization, as well as the level of HDAC6 expression within brain regions are reviewed and compared to the other HDAC isoforms. In various neurodegenerative diseases, the mechanisms underlying HDAC6 interaction with other proteins seem to be a promising approach in understanding the modulation of HDAC6 activity.

Published
2013

17. Sleep Deprivation Impairs Spatial Retrieval but Not Spatial Learning in the Non-Human Primate Grey Mouse Lemur

Author

Rahman, Anisur, primary, Languille, Solène, additional, Lamberty, Yves, additional, Babiloni, Claudio, additional, Perret, Martine, additional, Bordet, Regis, additional, Blin, Olivier J., additional, Jacob, Tom, additional, Auffret, Alexandra, additional, Schenker, Esther, additional, Richardson, Jill, additional, Pifferi, Fabien, additional, and Aujard, Fabienne, additional

Published
2013
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18. Sub-Anesthetic Ketamine Modulates Intrinsic BOLD Connectivity Within the Hippocampal-Prefrontal Circuit in the Rat.

Author

Gass, Natalia, Schwarz, Adam James, Sartorius, Alexander, Schenker, Esther, Risterucci, Celine, Spedding, Michael, Zheng, Lei, Meyer-Lindenberg, Andreas, and Weber-Fahr, Wolfgang

Subjects
KETAMINE, ELECTROENCEPHALOGRAPHY, SCHIZOPHRENIA, SPRAGUE Dawley rats, HALLUCINOGENIC drugs
Abstract

Dysfunctional connectivity within the hippocampal-prefrontal circuit (HC-PFC) is associated with schizophrenia, major depression, and neurodegenerative disorders, and both the hippocampus and prefrontal cortex have dense populations of N-methyl-D-aspartate (NMDA) receptors. Ketamine, a potent NMDA receptor antagonist, is of substantial current interest as a mechanistic model of glutamatergic dysfunction in animal and human studies, a psychotomimetic agent and a rapidly acting antidepressant. In this study, we sought to understand the modulatory effect of acute ketamine administration on functional connectivity in the HC-PFC system of the rat brain using resting-state fMRI. Sprague-Dawley rats in four parallel groups (N=9 per group) received either saline or one of three behaviorally relevant, sub-anesthetic doses of S-ketamine (5, 10, and 25 mg/kg, s.c.), and connectivity changes 15- and 30-min post-injection were studied. The strongest effects were dose- and exposure-dependent increases in functional connectivity within the prefrontal cortex and in anterior-posterior connections between the posterior hippocampus and retrosplenial cortex, and prefrontal regions. The increased prefrontal connectivity is consistent with ketamine-induced increases in HC-PFC electroencephalographic gamma band power, possibly reflecting a psychotomimetic aspect of ketamine's effect, and is contrary to the data from chronic schizophrenic patients suggesting that ketamine effect does not necessarily parallel the disease pattern but might rather reflect a hyperglutamatergic state. These findings may help to clarify the brain systems underlying different dose-dependent behavioral profiles of ketamine in the rat. [ABSTRACT FROM AUTHOR]

Published
2014
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19. Protocol for a systematic review of guidelines for rigour in the design, conduct and analysis of biomedical experiments involving laboratory animals.

Author

Vollert J, Schenker E, Macleod M, Bespalov A, Wuerbel H, Michel MC, Dirnagl U, Potschka H, Wever KE, Steckler T, Altevogt B, and Rice ASC

Abstract

Objective: Within the last years, there has been growing awareness of the negative repercussions of unstandardized planning, conduct and reporting of preclinical and biomedical research. Several initiatives have set the aim of increasing validity and reliability in reporting of studies and publications, and publishers have formed similar groups. Additionally, several groups of experts across the biomedical spectrum have published experience and opinion-based guidelines and guidance on potential standardized reporting. While all these guidelines cover reporting of experiments, an important step prior to this should be rigours planning and conduction of studies. The aim of this systematic review is to identify and harmonize existing experimental design, conduct and analysis guidelines relating to internal validity and reproducibility of preclinical animal research. The review will also identify literature describing risks of bias pertaining to the design, conduct and analysis of preclinical biomedical research., Search Strategy: PubMed, Embase and Web of Science will be searched systematically to identify guidelines published in English language in peer-reviewed journals before January 2018 (box 1). All articles or systematic reviews in English language that describe or review guidelines on the internal validity and reproducibility of animal studies will be included. Google search for guidelines published on the websites of major funders and professional organisations can be found in (Box 2)., Screening and Annotation: Unique references will be screened in two phases: screening for eligibility based on title and abstract, followed by screening for definitive inclusion based on full text. Screening will be performed in SyRF (http://syrf.org.uk). Each reference will be randomly presented to two independent reviewers. Disagreements between reviewers will be resolved by additional screening of the reference by a third, senior researcher., Data Management and Reporting: All data, including extracted text and guidelines, will be stored in the SyRF platform. Elements of the included guidelines will be identified using a standardized extraction form. Reporting will follow the PRISMA guidelines as far as applicable., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2018. Re-use permitted under CC BY. Published by BMJ.)

Published
2018
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20. Deficits of psychomotor and mnesic functions across aging in mouse lemur primates.

Author

Languille S, Liévin-Bazin A, Picq JL, Louis C, Dix S, De Barry J, Blin O, Richardson J, Bordet R, Schenker E, Djelti F, and Aujard F

Abstract

Owing to a similar cerebral neuro-anatomy, non-human primates are viewed as the most valid models for understanding cognitive deficits. This study evaluated psychomotor and mnesic functions of 41 young to old mouse lemurs (Microcebus murinus). Psychomotor capacities and anxiety-related behaviors decreased abruptly from middle to late adulthood. However, mnesic functions were not affected in the same way with increasing age. While results of the spontaneous alternation task point to a progressive and widespread age-related decline of spatial working memory, both spatial reference and novel object recognition (NOR) memory tasks did not reveal any tendency due to large inter-individual variability in the middle-aged and old animals. Indeed, some of the aged animals performed as well as younger ones, whereas some others had bad performances in the Barnes maze and in the object recognition test. Hierarchical cluster analysis revealed that declarative-like memory was strongly impaired only in 7 out of 25 middle-aged/old animals. These results suggest that this analysis allows to distinguish elder populations of good and bad performers in this non-human primate model and to closely compare this to human aging.

Published
2015
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