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I am passionate about the understanding of the neurobiological bases of nociception. In particular, I am interested in the power of our mind to affect how much pain we perceive.​ To do so, I bring together newest techniques to dissect anatomically and functionally pain circuity. Initial description of those pathways in health is crucial to understand their malfunctioning in pathology. 
I start with surgical transgene delivery to molecularly-defined discreet neuronal populations with the aid of certain viruses (AAVs). Then, by crossing optogenetic mapping, in vivo electrophysiology and calcium imaging, securely in anaesthetised animals, I gain the information about the functioning of those discreet pathways. The same neuronal tissue is then made light-transparent (CLARITY) and imaged for precise anatomical definition. Next, the candidate pathway is modulated using opto- or chemogenetics (DREADDs) in behaving animals. Here, affective cues (like fatigue, acute or chronic stress) are often added. Finally, this comprehensive approach is used to address outstanding questions in disease conditions.
 
See some of my current and past projects described in details below:
Coeruleospinal circuit

Coeruleospinal circuit

Distinct brainstem to spinal cord noradrenergic pathways inversely regulate spinal neuronal activity

DNIC in Bone Cancer

DNIC in Bone Cancer

The Stage-Specific Plasticity of Descending Modulatory Controls in a Rodent Model of Cancer-Induced Bone Pain

Bone cancer pain

Bone cancer pain

The impact of bone cancer on the peripheral encoding of mechanical pressure stimuli

Pain inhibits pain

Pain inhibits pain

Irritable nociceptors

Irritable nociceptors

Peripheral input drives spontaneous thalamic discharges, but not spinal DDH WDR in neuropathic rats.

Tuning in C-

Tuning in C-

Low‐intensity sinusoidal electrical stimulation paradigm to preferentially activate C‐fibers

Stress vs. stress

Stress vs. stress

The reduced level of growth factors in an animal model of depression is accompanied by regulated necrosis in the frontal cortex but not in the hippocampus.

Chronic stress HPA

Chronic stress HPA

Chronic mild stress influences nerve growth factor through a matrix metalloproteinase-dependent mechanism

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