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Christelle Anaclet PhD

TitleAssistant Professor
InstitutionUniversity of Massachusetts Medical School
DepartmentNeurobiology
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    Other Positions
    InstitutionUMMS - School of Medicine
    DepartmentNeurobiology

    InstitutionUMMS - School of Medicine
    DepartmentNeuroNexus Institute

    InstitutionUMMS - Graduate School of Biomedical Sciences
    DepartmentMD/PhD Program

    InstitutionUMMS - Graduate School of Biomedical Sciences
    DepartmentNeuroscience


    Collapse Biography 
    Collapse education and training
    Claude Bernard University Lyon 1, Lyon, , FranceBSBiochemistry
    Claude Bernard University Lyon 1, Lyon, , FranceMSNeuroscience
    Claude Bernard University Lyon 1, Lyon, , FrancePHD
    Collapse awards and honors
    2006Merit based travel award, SFRMS (Société Française de Recherche et de Médecine du Sommeil)
    2007Merit based travel award, European Histamine Research Society
    2010Young Investigator Award, 1st prize, European Histamine Research Society European Sleep Research Society
    2013Merit based travel award, Sleep Research Society
    2013Most Notable Publications in Sleep 2012, Sleep Research Society
    2014 - 2019K99/R00 Career Transition Award, National Institute of Mental Health
    2015Young Investigator Award, Sleep Research Society
    2017 - 2019Top 2017 Alzheimer’s research grant, Coins for Alzheimer’s Research Trust

    Collapse Overview 
    Collapse overview

    Anaclet Lab focuses on the neurophysiology of sleep, the involvement of slow-wave sleep (SWS) in cognitive functions and the development of new interventional strategies to treat sleep-wake and circadian disorders as well as sleep loss consequences. My research combines an innovative conceptual framework for how the brain sleeps with novel, cutting-edge tools, techniques and animal models to perform this work.


    Significance


    The National Institutes of Health estimates that sleep-related problems affect 50 to 70 million Americans and this transcends age, gender, and socioeconomic groupings. Sleep disruption has been implicated in neuropsychiatric disorders, linked with decreased cognitive and psychomotor function and is associated with increased cancer incidence. More recent evidence has strongly implicated sleep disruption in the pathogenesis of several metabolic disorders, heart disease and obesity – all of which represent long-term targets of the Department of Health and Human Services and other public health agencies. Sleep disturbances are also thought to contribute significantly to the disease burden in many neurodegenerative disorders, including Parkinson's and Alzheimer's disease, by disrupting activity cycles and impairing cognition. Given the tremendous economic and health burden of sleep-wake, neuropsychiatric and neurodegenerative disorders, understanding the “neurocircuit” basis of sleep regulation is not only a major health priority but is central to the development of novel pharmacologic and interventional strategies. The two major ongoing areas of research in my laboratory are:


    Studying the neuronal circuitry regulating the sleep-wake cycle


    The sub-cortical structures regulating sleep-wake cycle and its electroencephalogram (EEG) correlates are incompletely understood. One model of sleep–wake regulation posits a “flip-flop” switching mechanism that involves mutually inhibitory interactions between sleep-promoting neurons in the ventrolateral preoptic area (VLPO) and wake-promoting neurons in the brainstem as well as the forebrain (Saper et al., Neuron 2010). With our recent discovery of the SWS-promoting parafacial zone, the field has not only gained a more accurate picture of the sleep-promoting areas of the flip-flop mechanism but also reconciled earlier findings suggesting the existence of a potent SWS-promoting/EEG synchronizing “center” in the lower brainstem of mammals.


    Investigating the role of sleep in cognition


    It is now generally accepted that sleep is important for normal and/or optimal cognitive function. However, the interrelationship between sleep and cognition remains incompletely understood. There is accumulating evidence suggesting that both deep sleep—otherwise known as slow-wave-sleep (SWS)—and cortical slow-wave-activity (SWA, 0.5-4 Hz) critically subserve cognitive function, in particular learning and memory. For example, SWS deprivation produces cognitive dysfunction and increased local (cortical) SWA is observed following learning tasks that link to these cortical regions. Thus far, however, the role of sleep in cognition has been studied using models of sleep deprivation that either 1) fail to discriminate the respective role of SWS and rapid-eye-movement (REM) sleep in cognition, or 2) are not designed or otherwise able to determine if increased SWS and SWA might, in fact, reverse or alleviate cognitive dysfunction. By either opto- or chemo-genetically stimulating the PZ, we have been able to exclusively promote SWS particularly enriched in SWA which we believe will permit the unprecedented ability to link (or uncouple) SWS and cortical SWA with cognition function and memory consolidation.



    Collapse Rotation Projects

    The Anaclet lab studies the neuronal circuitry regulating of sleep-wake cycle, using behavioral monitoring, chemogenetics, neuronal circuit tracing and patch-clamp electrophysiology.


    A variety of potential rotation projects centered around the exploration of how and why sleep is necessary for survival. As projects are always evolving, I encourage students to contact the lab directly to discuss your specific interests.




    Collapse Research 
    Collapse research activities and funding
    K99MH103399     (ANACLET, CHRISTELLE)Jul 9, 2014 - Jun 30, 2016
    NIH
    Medullary Circuitry Regulating Slow-Wave-Sleep
    Role: Principal Investigator

         (Anaclet, Christelle)Jul 1, 2017 - Jun 30, 2019
    Coins for Alzheimer’s Research Trust
    Sleep Enhancement: A Strategy to Improve Cognitive Performance in Adult and Alzheimer’s Disease Mouse Models
    Role: PI

    Collapse Bibliographic 
    Collapse selected publications
    Publications listed below are automatically derived from MEDLINE/PubMed and other sources, which might result in incorrect or missing publications. Faculty can login to make corrections and additions.
    List All   |   Timeline
    1. Anaclet C, Griffith K, Fuller PM. Activation of the GABAergic Parafacial Zone Maintains Sleep and Counteracts the Wake-Promoting Action of the Psychostimulants Armodafinil and Caffeine. Neuropsychopharmacology. 2017 Jul 19. PMID: 28722021.
      View in: PubMed
    2. Anaclet C, Fuller PM. Brainstem regulation of slow-wave-sleep. Curr Opin Neurobiol. 2017 May 10; 44:139-143. PMID: 28500870.
      View in: PubMed
    3. Venner A, Anaclet C, Broadhurst RY, Saper CB, Fuller PM. A Novel Population of Wake-Promoting GABAergic Neurons in the Ventral Lateral Hypothalamus. Curr Biol. 2016 Aug 22; 26(16):2137-43. PMID: 27426511.
      View in: PubMed
    4. Anaclet C, Pedersen NP, Ferrari LL, Venner A, Bass CE, Arrigoni E, Fuller PM. Basal forebrain control of wakefulness and cortical rhythms. Nat Commun. 2015 Nov 03; 6:8744. PMID: 26524973.
      View in: PubMed
    5. Anaclet C, Ferrari L, Arrigoni E, Bass CE, Saper CB, Lu J, Fuller PM. The GABAergic parafacial zone is a medullary slow wave sleep-promoting center. Nat Neurosci. 2014 Sep; 17(9):1217-24. PMID: 25129078.
      View in: PubMed
    6. Gondard E, Anaclet C, Akaoka H, Guo RX, Zhang M, Buda C, Franco P, Kotani H, Lin JS. Enhanced histaminergic neurotransmission and sleep-wake alterations, a study in histamine H3-receptor knock-out mice. Neuropsychopharmacology. 2013 May; 38(6):1015-31. PMID: 23303066.
      View in: PubMed
    7. Anaclet C, Lin JS, Vetrivelan R, Krenzer M, Vong L, Fuller PM, Lu J. Identification and characterization of a sleep-active cell group in the rostral medullary brainstem. J Neurosci. 2012 Dec 12; 32(50):17970-6. PMID: 23238713.
      View in: PubMed
    8. Anaclet C, Zhang M, Zhao C, Buda C, Seugnet L, Lin JS. Effects of GF-015535-00, a novel a1 GABA A receptor ligand, on the sleep-wake cycle in mice, with reference to zolpidem. Sleep. 2012 Jan; 35(1):103-11. PMID: 22215924.
      View in: PubMed
    9. Krenzer M, Anaclet C, Vetrivelan R, Wang N, Vong L, Lowell BB, Fuller PM, Lu J. Brainstem and spinal cord circuitry regulating REM sleep and muscle atonia. PLoS One. 2011; 6(10):e24998. PMID: 22043278.
      View in: PubMed
    10. Lin JS, Anaclet C, Sergeeva OA, Haas HL. The waking brain: an update. Cell Mol Life Sci. 2011 Aug; 68(15):2499-512. PMID: 21318261.
      View in: PubMed
    11. Sakai K, Takahashi K, Anaclet C, Lin JS. Sleep-waking discharge of ventral tuberomammillary neurons in wild-type and histidine decarboxylase knock-out mice. Front Behav Neurosci. 2010; 4:53. PMID: 21060718.
      View in: PubMed
    12. Anaclet C, Pedersen NP, Fuller PM, Lu J. Brainstem circuitry regulating phasic activation of trigeminal motoneurons during REM sleep. PLoS One. 2010 Jan 20; 5(1):e8788. PMID: 20098748.
      View in: PubMed
    13. Anaclet C, Parmentier R, Ouk K, Guidon G, Buda C, Sastre JP, Akaoka H, Sergeeva OA, Yanagisawa M, Ohtsu H, Franco P, Haas HL, Lin JS. Orexin/hypocretin and histamine: distinct roles in the control of wakefulness demonstrated using knock-out mouse models. J Neurosci. 2009 Nov 18; 29(46):14423-38. PMID: 19923277.
      View in: PubMed
    14. Guo RX, Anaclet C, Roberts JC, Parmentier R, Zhang M, Guidon G, Buda C, Sastre JP, Feng JQ, Franco P, Brown SH, Upton N, Medhurst AD, Lin JS. Differential effects of acute and repeat dosing with the H3 antagonist GSK189254 on the sleep-wake cycle and narcoleptic episodes in Ox-/- mice. Br J Pharmacol. 2009 May; 157(1):104-17. PMID: 19413575.
      View in: PubMed
    15. Lin JS, Dauvilliers Y, Arnulf I, Bastuji H, Anaclet C, Parmentier R, Kocher L, Yanagisawa M, Lehert P, Ligneau X, Perrin D, Robert P, Roux M, Lecomte JM, Schwartz JC. An inverse agonist of the histamine H(3) receptor improves wakefulness in narcolepsy: studies in orexin-/- mice and patients. Neurobiol Dis. 2008 Apr; 30(1):74-83. PMID: 18295497.
      View in: PubMed
    16. Ligneau X, Landais L, Perrin D, Piriou J, Uguen M, Denis E, Robert P, Parmentier R, Anaclet C, Lin JS, Burban A, Arrang JM, Schwartz JC. Brain histamine and schizophrenia: potential therapeutic applications of H3-receptor inverse agonists studied with BF2.649. Biochem Pharmacol. 2007 Apr 15; 73(8):1215-24. PMID: 17343831.
      View in: PubMed
    17. Parmentier R, Anaclet C, Guhennec C, Brousseau E, Bricout D, Giboulot T, Bozyczko-Coyne D, Spiegel K, Ohtsu H, Williams M, Lin JS. The brain H3-receptor as a novel therapeutic target for vigilance and sleep-wake disorders. Biochem Pharmacol. 2007 Apr 15; 73(8):1157-71. PMID: 17288995.
      View in: PubMed
    18. Brabant C, Quertemont E, Anaclet C, Lin JS, Ohtsu H, Tirelli E. The psychostimulant and rewarding effects of cocaine in histidine decarboxylase knockout mice do not support the hypothesis of an inhibitory function of histamine on reward. Psychopharmacology (Berl). 2007 Feb; 190(2):251-63. PMID: 17072589.
      View in: PubMed
    19. Ligneau X, Perrin D, Landais L, Camelin JC, Calmels TP, Berrebi-Bertrand I, Lecomte JM, Parmentier R, Anaclet C, Lin JS, Bertaina-Anglade V, la Rochelle CD, d'Aniello F, Rouleau A, Gbahou F, Arrang JM, Ganellin CR, Stark H, Schunack W, Schwartz JC. BF2.649 [1-{3-[3-(4-Chlorophenyl)propoxy]propyl}piperidine, hydrochloride], a nonimidazole inverse agonist/antagonist at the human histamine H3 receptor: Preclinical pharmacology. J Pharmacol Exp Ther. 2007 Jan; 320(1):365-75. PMID: 17005916.
      View in: PubMed
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