Conditions like anaerobic exercise, sickle cell anemia, peripheral vascular disease and other cardiovascular disorders cause changes in protective sympathetic reflexes which are thought to be mediated by group III and IV muscle sensory neurons. However, these same fibers are also likely playing a role in ischemic muscle pain associated with these conditions. We do not currently have a comprehensive understanding of the sensitization that occurs in individual muscle afferent subtypes after ischemia or how changes in gene expression in the sensory ganglia may affect muscle afferent sensitization, which in turn may lead to the initiation or progression of pain states.
The goal of this project is to functionally characterize group III and IV muscle afferents in preclinical models of peripheral ischemia and determine the molecular mechanisms involved with changes in specific subpopulations of muscle afferents. The information from these studies will provide a novel way to allow us to better understand the functional implications of changes in muscle sensory neurons and could be used to develop new and more appropriate therapeutic approaches for the management of altered cardiovascular reflexes and/or chronic musculoskeletal pain associated with ischemia.
MP Jankowski- Principal Investigator
2012 International Association for the Study of Pain Early Career Grant
2012- American Pain Society and the Rita Allen Foundation Award in Pain
||Neurochemical identity, central anatomy and response properties of an individually characterized muscle sensory neuron.
||Ischemia causes skeletal muscle atrophy and tissue degradation.