Graziella Di Cristo , Ph.D.
    Graziella Di Cristo
    Research Axis
    Brain and Child Development
    Research Theme
    Neurodevelopmental diseases

    514 345-4931 #2867

    514 345-4801


    Internship opportunity(ies)


    • Postdoctoral Fellow in Neuroscience, Cold Spring Harbor Laboratory, NY, USA, 2001-2006.
    • PhD in Neuroscience, University of Pisa, Italy, 1998-2001.

    Research Interests

    In the cerebral cortex, neural networks consist of two broad classes of neurons: excitatory projection neurons, which use glutamate as neurotransmitter, and inhibitory local-circuit interneurons, comprising about 20-30% of all cortical neurons, which primarily use gamma-aminobutyric acid-GABA as a neurotransmitter. Although a minor cell population compared to glutamatergic neurons, GABAergic interneurons play a vital role in modulating neuronal excitability and integration, and in the generation of temporal synchrony and oscillations among networks of glutamatergic neurons. In addition, the development of GABAergic inhibition has recently been shown to play a key role in critical period plasticity of cortical circuits. Critical periods represent epochs of heightened brain plasticity during which experience can produce permanent, large-scale changes in neuronal circuits. By regulating critical period plasticity, GABAergic interneurons may influence how experience shapes the brain during early life and adolescence. To date our understanding of the molecular mechanisms regulating GABAergic synapse development is still in its infancy.

    Disruption of the balance between excitatory and inhibitory synaptic activities is believed to cause diseases such as epilepsy, autism and schizophrenia. Alteration in the maturation of the GABAergic network thus might be a critical determinant of these neurodevelopmental disorders. Understanding the cellular and molecular mechanisms governing GABAergic circuit development is the first essential step towards a better comprehension of how abnormalities in this process can occur, thereby leading to aberrant cortical development and function. The overall goal of my laboratory is to study the molecular mechanisms regulating GABAergic synapse development, by using a combination of molecular, imaging and electrophysiological techniques.

    We currently focus on the following three questions:

    • Molecular pathways regulating GABAergic synapse maturation in the postnatal brain;
    • Mechanisms linking experience to GABAergic synapse maturation in primary visual cortex;
    • Alterations of GABAergic circuit development in animal models of neurodevelopment diseases (e.g. epilepsy).

    Awards and Distinctions

    • Canada Research Chair in Neural Circuit Development, Tier 2, 2006-2011.
    • Young Investigator Award, National Alliance for Research on Schizophrenia and Depression (NARSAD), 2007-2009.
    • Young Investigator Award, NARSAD, 2004-2006.
    • Postdoctoral Fellowship, European Molecular Biology Organization, 2002-2004.
    • Graduate Fellowship, Scuola Normale Superiore, 1997-2000.

    Most Important Publications

    1. Di Cristo G, Chattopadhyaya B, Kuhlman SJ, Fu Y, Bélanger M-C*, Wu CZ Rutishauser U, Maffei L, Huang ZJ (2007). Activity-dependent PSA expression promotes the maturation of GABA inhibition and the onset of critical period plasticity. Nature Neuroscience,10:1569-1577.
    1. Gibbs SA*, Chattopadhyaya B*, Desgent S, Awad PN, Clerk-Lamalice O, Levesque M, Vianna RM, Rébillard RM, Delsemme AA, Hébert D, Tremblay L, Descarries L, Lepage M, Di Cristo  G, Carmant L (2011). Long-term consequences of a prolonged febrile seizure in a dual pathology model. Neurobiology of Diseases, 43(2):312-21. * equal contribution
    1. Bélanger M-C, Di Cristo G (2011). Sensory experience differentially modulates the mRNA expression of the polysialyltransferases ST8SiaII and ST8SiaIV in postnatal mouse visual cortex. PloSOne, 2011;6(9):e24874.
    1. Baho E, Di Cristo G (2012). Synaptic activity is required for the maintenance of GABAergic innervation patterns in the cortex. Journal of Neuroscience 32:911-8.
    1. Chattopadhyaya B, Baho E, Schachner M, Huang JZ, Di Cristo G (2013). NCAM-mediated Fyn signaling promotes perisomatic GABAergic synapse maturation in adolescent cortex. Journal of Neuroscience, 33:5957-68.
    1. Berryer MH, Hamdan FF, KlittenLL, Møller RS, Carmant L, Patry P, Dobrzeniecka S, Rochefort D, Neugnot M, Lacaille JC, Niu Z, Eng CM, Yang Y, Palardy S, Céline Belhumeur C, Rouleau GA, Tommerup N, Immken LD, Beauchamp M, Simpson Patel G, Scheffzek K, Hjalgrim H, Michaud JL, Di Cristo G (2013). Mutations in SYNGAP1 cause intellectual disability, autism and a specific form of epilepsy by inducing haploinsufficiency. Human Mutations 34:385-94.
    1. Lachance-Touchette P*, Choudhury M*, Stoica A, Di Cristo G, Cossette P (2014). Single-cell genetic expression of mutant GABAA receptors causing Human genetic epilepsy alters dendritic spine and GABAergic bouton formation in a mutation-specific manner. Front Cell Neurosci. 2014 Oct 14;8:317. doi: 10.3389/fncel.2014.00317. * equal contribution.
    1. Awad PN, Sanon N, Chattopadhyaya B, Carriço JN, Ouardouz M, Gagné J, Duss S, Wolf D, Desgent S, Cancedda L, Carmant L, Di Cristo G (2016). Reducing premature KCC2 expression rescues seizure susceptibility and spine morphology in atypical febrile seizures. .Neurobiology of Diseases, 91:10-20.
    1. Berryer MH, Chattopadhyaya B, Xing P, Antoine-Bertrand J, Lévesque M, Sanon N, Bosoi C, Fadi F, Hamdan FF, Boucher B, Carmant L, Avoli M, Lamarche-Vane N, Lacaille J-C, Michaud JL, Di Cristo G (2016). Syngap1 deficit in GABAergic cells impairs synaptic development, functional inhibition and cognitive abilities. Nature Communications, 7:13340
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Created on 9/18/2014
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