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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.
Project GoalThe 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
Funding:2013-1R01AR064551 (NIH/NIAMS)2012 International Association for the Study of Pain Early Career Grant2012- American Pain Society and the Rita Allen Foundation Award in Pain
Surgery, preventative medicine and neonatal intensive care in addition to various pathological disorders in children can all lead to painful conditions making pediatric pain a significant clinical problem. Many of the pain therapies used in children are similar to that used in adults, yet it is well known that use of certain pharmacotherapies such as opiates or anti-inflammatories in children can have serious adverse effects.
Project GoalThe goal of this project is to comprehensively phenotype both cutaneous and muscle afferents during development and then determine the molecular mechanisms of sensitization that may occur after neonatal insults such as inflammation or ischemia. These studies will not only allow us to obtain a significant amount of information on sensory neuron development, but will also inform us about the types of sensitization that occurs after neonatal injury and how this may alter sensory neuron responses later in life. This information may provide insight into the development of more appropriate pain therapies that target primary afferents in children.
Funding2013-Trustee Scholar Award (CCHMC)2013- 1R03HD077483 (NIH/NICHD)
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