Mechanical allodynia is a painful symptom evoked by normally harmless stimulation, such as light pressure or friction. It results in patients from tissue damage/inflammation (inflammatory pain) or damage to the nervous system (neuropathic pain). We know that in all of these conditions, hypersensitivity to pain at the site of injury (called primary hyperalgesia) results from sensitization of sensory nociceptors (peripheral sensitization). In contrast, secondary hyperalgesia, i.e. mechanical allodynia that occurs in adjacent normal tissues, results from impaired information processing in the central nervous system (CNS) (central sensitization) . Thus, during mechanical allodynia, innocuous mechanical information is pathologically converted into nociceptive information within the CNS, generating pain. Numerous works, notably by the team, suggest that this “conversion” of touch into pain occurs initially at the level of the neural networks of the spinal and medullary dorsal horn, then extending to the cortical and subcortical regions of the brain.

The general objective of this axis is to understand the mechanisms of mechanical allodynia and to reveal new molecular targets, in order to develop new agents to treat this pain symptom. We address the following questions by combining preclinical and clinical approaches:

Which sensory afferents, among the low-threshold mechanoreceptor (LTMR) family, are involved in the transmission of mechanical information that is converted into pain during allodynia?

Which neurons specifically participate in the neural circuits of the dorsal horn involved in mechanical allodynia of neuropathic or inflammatory origin?

What molecular cascades lead to chronic pain within these circuits?

How does mechanical allodynia spread to uninjured territories?