I was born in Brittany, a cultural region in the northwest of France. I grew up in Rennes, its capital, where I obtained my BSc Degree with special emphasis on physiology, in 2005. In 2006, I went to Marseille in the southeast of France and I joined the Laboratory of Neurobiology and Cognition, where I obtained my MSc degree in Neuroscience in 2007 and completed my PhD, in 2011, under the supervision of Dr Paul Apicella.

During my PhD, I studied the role of the striatum (STR), which correspond to the main input structure of the Basal Ganglia (BG), in the expression of motor skills and habits, such as lacing shoes, biking, typing. To do that, I examined the respective contribution of the different neuronal components of the STR, by single-unit recording methods in awake monkey, in the processes underlying the expression of automatic motor sequences.

Benefiting from this experience, at the beginning of 2012, I joined the laboratory of Pr Hagai Bergman at the Hebrew University of Jerusalem, as postdoctoral fellow, in order to extend my understanding of the role of BG in non-motor processes and more particularly the contribution of the subthalamic nucleus (STN) which is the second input structure of the BG. Interestingly, it must be stressed that Deep Brain Stimulation of STN (STN-DBS) is the preferred surgical treatment for advanced Parkinson's disease (PD). However, among PD patients undergoing STN-DBS, few of them develop cognitive and motivational/emotional troubles such as gambling, sexual addiction. Thus, the emergence of these non-motor side effects after STN-DBS point out the absolute necessity to improve and precise our knowledge about the involvement of the STN in cognitive and motivational/emotional processes. To address this issue, my experimental approach is to record the neuronal activity in the STN of monkeys while they are engaged in behavioral task that require processing of information relative to appetitive and aversive events. Electrophysiological recordings will be carried out before and after treatment by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a neurotoxin that causes permanent symptoms of PD, by destroying midbrain dopaminergic neurons. As a consequence, expected results should provide new insight about the contribution of the STN in the processing of motivational information, during healthy state, at the neuronal scale and permit to better understand how the dysregulation of STN activity associated with the physiopathology of PD affect the processing of this kind of non-motor information.

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