PhD student in Medicine
Award-winning publication: Enhancing K–Cl co-transport restores normal spinothalamic sensory coding in a neuropathic pain model
Published in: BRAIN, 137; 724-738, 2014
"Our findings are especially significant since they respond to key issues in pain that have been the focus of much debate in the past 50 years: how is pain encoded in the spinal cord and how is it transmitted to the brain physiologically and pathologically? Our study answers these questions and identifies the cellular and mechanistic substrates involved in the development of tactile allodynia (pain triggered by stimulus that normally does not cause pain), one of the most debilitating symptoms of chronic pain. The study demonstrates that modifying the capacity to expulse chloride ions by decreasing potassium chloride cotransporter KCC2 concentrations in a specific sub-population of spinothalamic neurons causes tactile allodynia. Using an animal model of chronic pain, we also proved that a positive modulation of the cotransporter with the new CLP257 compound normalizes the encoding of this sub-population of spinothalamic neurons."
Chronic pain is often unresponsive to treatment options, which generally only provide a certain level of relief. The findings of this study and others have uncovered a very promising potential pharmacological target for the treatment of chronic pain. This new avenue is very timely since an inadequate understanding of the physiopathology of chronic pain has significantly limited pharmacological development. In addition, recent data tends to associate the mechanism identified by Guillaume Lavertu with several neurological and psychiatric disorders, including epilepsy, stress, spasticity, schizophrenia, autism and addiction. These findings are expected to give rise to a range of new therapeutic approaches.