Grants and Contracts Details
Description
Work performed during the previous funding periods indicates that intrathecal administration of NPY reduces
the mechanical and thermal hypersensitivity associated with inflammation or nerve injury. The objective of the
present application is to establish NPY as an endogenous pain modulator, and to identify the mechanisms
underlying NPY-mediated inhibition of inflammatory or neuropathic pain. The central hypothesis is that tissue
or nerve injury sensitizes the dorsal horn to the pain inhibitory actions of NPY receptor signaling. Our approach
involves transgenic, biochemical, neurophysiological, anatomical, and behavioral methods to determine: the
anti-allodynic actions of endogenous NPY (Aim 1); the effect of injury on NPY receptor coupling to G-proteins
(Aim 2); the effect of injury on the inhibition by NPY of SP release and subsequent NK1 receptor (NK1)
activation in the spinal cord (Aim 3A); and the effect of NPY on the activity of spinal neurons that express the
NPY Y1 receptor (Aim 3B). Our long-term goal is to understand endogenous neuropeptidergic inhibition of
spinal pain transmission, and to establish the therapeutic potential of NPY receptor agonists for chronic pain.
Status | Finished |
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Effective start/end date | 9/10/02 → 1/31/15 |
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