Grant: Project Grant

We have all experienced muscle pain in our life, whether after strenuous or eccentric exercise or just repetition of unaccustomed movements. The pain following these movements is caused by minor damage or inflammation to the muscle and is usually not felt at rest. The soreness or tenderness perceived upon palpation of the exercised muscle or an attempt to move is usually considered as a subclinical situation since it is short lasting and recess by itself without need for treatment. However, in some people it leads to a debilitating chronic condition where the pain eventually spreads to several muscles rendering movements very difficult and sometimes even just contact with objects like a chair or a bed become painful. Normally, painful stimuli activate the nerve endings of specialized sensory neurons that inform the brain of their presence. Every type of sensory neuron is specialized for the type of stimuli it is designed to detect. Sensory neurons in the eye detect light but not sound, for instance. In a previous study, we made small injections (2 injections, 2 days apart) of an acidic solution into muscles to mimic, in an animal model, the changes that occur in muscles that are slightly damaged or inflamed, and found that a type of sensory neuron, which is not normally associated to pain perception, becomes abnormally hyperactive. These sensory neurons should detect muscle stretch and not painful stimuli, but because the period of their hyperactivity lasted for as long as the muscle pain lasted in the animals, we asked if the two are related. The aim of this project is to understand the sequence of cellular events that leads to this abnormal activity and to understand how abnormal activity in these cells ends up causing the brain to feel pain instead of muscle stretch.