Deficits de récompense, GPCRs et sociabilité (DRuGS)
Our research is structured around three main axes:
1: To identify the neural and molecular substrates involved in the control of social behaviour and, in pathological conditions, in the etiology of Autism Spectrum Disorders (ASD),
2: To propose new pharmacological and/or behavioural approaches to facilitate or restore sociability, in a physiological or pathological context (autism),
3: To develop new pharmacological tools, in particular in the form of single-chain antibodies or nanobodies, targeting GPCRs of interest to understand their role in the control of social behaviour and/or to treat autistic symptoms.
Réferences:
Meng J, Xu C,Lafon P-A, Roux S, Mathieu M, Scholler P, Blanc E, Becker JAJ, Le Merrer J, Gonzales-Maeso J, Chames P, Liu J, Pin J-P, Rondard P. Optical biosensors of native membrane protein complexes reveal a high proportion of mGlu heterodimers in the brain. Nature Chemical Biology, 18(8):894-903.
Derieux C, Léauté A, Brugoux A, Jaccaz D, Terrier C, Pin J-P, Kniazeff J, Becker JAJ, Le Merrer J (2022). Chronic sodium bromide treatment relieves autistic-like behavioral deficits in three mouse models of autism. Neuropsychopharmacology, 47(9):1680-1692.
Laboute T, Gandía J, Pellissier LP, Corde Y, Rebeillard F, Gallo M, Gauthier C, Léauté A, Diaz J, Poupon A, Kieffer BL, Becker JA, Le Merrer J (2020). The orphan receptor GPR88 blunts the signaling of opioid receptors and multiple striatal GPCRs. Elife, 31;9:e50519 .
Pellissier LP, Gandia J, Laboute T, Becker JA, Le Merrer J (2017). Mu opioid receptor, social behaviour and autism spectrum disorder: reward matters. British Journal of Pharmacology, 175:2750-2769.
Becker JAJ, Clesse D, Spiegelhalter C, Schwab Y, Kieffer BL, Le Merrer J (2014). Autistic-like syndrome in mu opioid receptor null mice is relieved by facilitated mGluR4 activity. Neuropsychopharmacology, 39:2049-2060.
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