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REGULATION OF DEVELOPMENTAL NEUROGENESIS

 

 

Education and Training

  • M.Sc. in Neuroscience, University of Rouen, France, 2001
  • Ph.D. in Neuroscience, University of Rouen, France, 2005
  • Post-Doctoral Fellow, Department of Neuroscience and Cell Biology, Rutgers Robert Wood Johnson Medical School, Piscataway, NJ USA (Emanuel DiCiccoBloom's lab), 2005-08
  • Post-Doctoral Fellow, Laboratory of Cellular and Neuroendocrine Differenciation, University of Rouen, France (David Vaudry's lab), 2008-09

Holder of a Level I training in animal experimentation and trained on small mammal surgery.

Contact Information

Inserm U1239 – DC2N
CURIB Building
2nd floor, room 239
25, rue Tesnière
76821 Mont-Saint-Aignan
Telephone: +33(0)235 14 6641
Fax: +33(0)235 14 6946
E-mail: This email address is being protected from spambots. You need JavaScript enabled to view it.

 

 

 

Educational role:

 

-          Responsible of  Master 1 Biology & Health - Cell Imaging

-          Responsible of the 1st year in Life Technologies at ESITEch Engineering School

 

Research Areas: Mechanisms controlling neuronal fate and survival, brain wiring and function

 

Research

 

Many developmental disorders arise from abnormalities in neurotransmission, neuronal connectivity, and/or neuron/glia interactions. It is thus essential to elucidate the mechanisms underlying the establishment of neuronal networks, including cortical network, to propose new therapies or markers aiming at preventing the occurrence of such brain deficits in childs. Our group is focused on the function of Selenoprotein T during neurodevelopment, and its contribution to the regulation of redox homeostasis during the establishment of functional circuitry.

 

Our research unit has characterized Selenoprotein T as a Selenium-containing protein expressed in the central nervous system during development. Using genetic invalidation models in mice, we have demonstrated that this protein contributes to the control of redox homeostasis and neuroblast survival. These alterations detected in the knockout animals lead to behavioral deficits, which manifest in the absence of gross morphological abnormalities.

 

Murine models, supplemented with more specific approaches, such as in utero electroporation are being used to contribute deciphering the mechanisms underlying the complex origin of cognitive functions, and how they can be altered during pathophysiological conditions, such as ASD or ADHD.

 

        

 

Selected Publications

DiCicco-Bloom, E., Falluel-Morel,A., Developmental Neurogenesis, in : Reference Module in Neuroscience and Biobehavioral Psychology. Elsevier, ISBN 9780128093245 in press.

Castex, M.T., Arabo, A., Bénard, M., Roy, V., Le Joncour, V., Prévost, G., Bonnet, J.-J., Anouar, Y., Falluel-Morel, A., 2015. Selenoprotein T Deficiency Leads to Neurodevelopmental Abnormalities and Hyperactive Behavior in Mice. Mol. Neurobiol. 53:5818-5832

Boukhzar, L., Hamieh, A., Cartier, D., Tanguy, Y., Alsharif, I., Castex, M., Arabo, A., El Hajji, S., Bonnet, J.-J., Errami, M., Falluel-Morel, A., Chagraoui, A., Lihrmann, I., Anouar, Y., 2016. Selenoprotein T Exerts an Essential Oxidoreductase Activity That Protects Dopaminergic Neurons in Mouse Models of Parkinson’s Disease. Antioxid. Redox Signal. 24, 557–574.

Balland, E., Dam, J., Langlet, F., Caron, E., Steculorum, S., Messina, A., Rasika, S., Falluel-Morel, A., Anouar, Y., Dehouck, B., Trinquet, E., Jockers, R., Bouret, S.G., Prévot, V., 2014. Hypothalamic tanycytes are an ERK-gated conduit for leptin into the brain. Cell Metab. 19, 293–301.

Petit, A., Delaune, A., Falluel-Morel, A., Goullé, J.-P., Vannier, J.-P., Dubus, I., Vasse, M., 2013. Importance of ERK activation in As2O3-induced differentiation and promyelocytic leukemia nuclear bodies formation in neuroblastoma cells. Pharmacol. Res. 77, 11–21.

Prevost, G., Arabo, A., Jian, L., Quelennec, E., Cartier, D., Hassan, S., Falluel-Morel, A., Tanguy, Y., Gargani, S., Lihrmann, I., Kerr-Conte, J., Lefebvre, H., Pattou, F., Anouar, Y., 2013. The PACAP-regulated gene selenoprotein T is abundantly expressed in mouse and human β-cells and its targeted inactivation impairs glucose tolerance. Endocrinology 154, 3796–3806.

Falluel-Morel, A., Lin, L., Sokolowski, K., McCandlish, E., Buckley, B., DiCicco-Bloom, E., 2012. N-acetyl cysteine treatment reduces mercury-induced neurotoxicity in the developing rat hippocampus. J. Neurosci. Res. 90, 743–750.

Sokolowski, K., Falluel-Morel, A., Zhou, X., DiCicco-Bloom, E., 2011. Methylmercury (MeHg) elicits mitochondrial-dependent apoptosis in developing hippocampus and acts at low exposures. Neurotoxicology 32, 535–544.

Tanguy, Y., Falluel-Morel, A., Arthaud, S., Boukhzar, L., Manecka, D.-L., Chagraoui, A., Prevost, G., Elias, S., Dorval-Coiffec, I., Lesage, J., Vieau, D., Lihrmann, I., Jégou, B., Anouar, Y., 2011. The PACAP-regulated gene selenoprotein T is highly induced in nervous, endocrine, and metabolic tissues during ontogenetic and regenerative processes. Endocrinology 152, 4322–4335.

DiCicco-Bloom, E., Falluel-Morel, A., 2010. Developmental Neurogenesis, in: Encyclopedia of Behavioral Neuroscience. Elsevier, pp. 396–404.

 

Funding

            

 

Current Group Members

 

 

 

Alumni