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Friday Science Review: June 21, 2013

Arthritis is a highly prevalent disorder, affecting about 1 in 5 people in North America, and is characterized by joint inflammation, which results in pain and reduction in joint mobility. Underlying these symptoms is the release of a peptide called substance P, so called because of its role in signalling pain. New research published in the Journal of Neuroscience from the lab of Dr. Alfredo Ribeiro-da-Silva at McGill University indicates that joint pain associated with arthritis may be due in part to increased activation of substance P-releasing nerve cells caused by inappropriate sprouting of sympathetic nerve fibers. The authors induced arthritis, which was characterized by joint edema and increased pain responses, in the hind ankle joint of rats. Using immunohistochemistry, the authors found that sympathetic nerve fibers, which normally innervate blood vessels in the skin to regulate blood-flow, sprouted to innervate the synovial membrane surrounding the ankle joint and the upper dermis covering the ankle joint four weeks after the arthritic phenotype was induced. Interestingly, these newly sprouted sympathetic nerve fibers closely associated with peptidergic nerve cells, which release substance P and are associated with transmitting pain responses. This result suggests that sympathetic nerve sprouting can increase the activity of substance P-containing neurons, exaggerating pain responses and inflammation. Consistent with this, pharmacologically blocking sympathetic nerve responses in these rats shifted the pain threshold back near normal. The authors also found that the expression of mature nerve growth factor (NGF), which is necessary for sympathetic neuron growth and survival, was increased near the ankle joint in which arthritis had been induced. The authors suggest that activity of peptidergic nerve cells increases joint and skin inflammation which initiates an immune response leading to increased production of mature NGF. The increase in NGF leads to sympathetic nerve sprouting, a further increase in peptidergic nerve cell activity, and ultimately to hyperactive pain signaling. These findings suggest that decreasing the production of mature NGF near arthritic sites can decrease sympathetic nerve sprouting and reduce arthritis associated pain. Additionally, localized inhibition of sympathetic neurotransmission may be a way to provide short-term arthritis pain relief.

2 responses to “Friday Science Review: June 21, 2013

  1. Pingback: Friday Science Review: June 21, 2013 « Non Resource Report

  2. Pingback: Friday Science Review: June 21, 2013 | Vision 2050

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