Research and teaching
- Spinal Cord / Nerve Injury & Pain
Pain is a major symptom of inflammation. Following tissue damage or during pathological inflammation linked to chronic diseases such as arthritis, inflammatory bowel disease (IBD) or asthma, the primary afferent sensory neurons that sense nociceptive information (nociceptors) are exposed to inflammatory mediators. These molecules lower the threshold of activation of the nociceptor – a process called peripheral sensitization. We are investigating the molecular changes that occur in nociceptors during pain sensitization. Specifically, we are focusing on a family of ion channels called, Transient Receptor Potential (TRP) channels that are expressed in primary afferent neurons. Using multidisciplinary approach including molecular biology, imaging, electrophysiology, and rodent models of inflammatory pain we are investigating the post-translational regulation of TRP channels in this context. We are particularly interested in the signalling pathways that modulate the activation of TRP channels and their trafficking to and from the plasma membrane. Ion channels are important molecular targets in the treatment of several pathologies (cardiac arrhythmia, hypertension, epilepsy,…), thus the TRP channel family could represent a new class of targets for the treatment of inflammatory pain.
My teaching interests include the neurophysiology and anatomy of the pain signaling pathway, the molecular pharmacology of nociceptive ion channels: Voltage-Gated Na+ channels, Voltage-Gated Ca2+ channels and Transient Receptor Potential Channels (TRPV1-4, TRPA1, TRPM8). I also developed teaching interests in the regulation of these channels by inflammatory molecules and their receptors coupled to heteromeric G proteins. I contribute to teaching activities in the field of G protein-coupled receptors.