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Axonal Transport and Local Translation in Neuropathic Pain
July 1, 2011 to June 30, 2013
GRANT:
FederalFunding Status:
Completed ProjectFunding Agency:
National Institutes of Health (NIH)Funding Institute:
National Institute of Nursing ResearchGrant Number:
R00NR010797Published Grant:
NIH RePORTGoals
Neuropathic pain, the chronic pain experienced following injury, infection, or inflammation of peripheral nerves, sharply contrasts with normal pain, both is the molecular mechanisms which cause it and in their responses to conventional pain treatments. Current animal models of nerve trauma have provided some insights into the neuronal changes that occur in response to peripheral nerve damage - revealing a remarkable degree of plasticity in both the sensory neurons and spinal cord. Understanding how axonal transport and local protein synthesis contribute to increased hyperexcitability of these damaged sensory neurons may point to alternative methods of treating pathological pain states.