Peripheral hyperalgesia in experimental neuropathy: exacerbation by neuropeptide Y

DJ Tracey, MA Romm, NNL Yao - Brain research, 1995 - Elsevier
DJ Tracey, MA Romm, NNL Yao
Brain research, 1995Elsevier
Injury of peripheral nerves often results in hyperalgesia (an increased sensitivity to painful
stimuli). This hyperalgesia is mediated in part by sympathetic neurotransmitters. We
examined the effect of neuropeptide Y (NPY), specific Y1 and Y2 agonists, and an NPY
antagonist on peripheral hyperalgesia in rats whose sciatic nerves had been partially
transected. NPY and the Y2 agonist, N-acetyl [Leu28, Leu31] NPY 24–36 exacerbated both
mechanical and thermal hyperalgesia, while the Y1 agonist,[Leu31, Pro34] NPY relieved …
Injury of peripheral nerves often results in hyperalgesia (an increased sensitivity to painful stimuli). This hyperalgesia is mediated in part by sympathetic neurotransmitters. We examined the effect of neuropeptide Y (NPY), specific Y1 and Y2 agonists, and an NPY antagonist on peripheral hyperalgesia in rats whose sciatic nerves had been partially transected. NPY and the Y2 agonist, N-acetyl [Leu28,Leu31] NPY 24–36 exacerbated both mechanical and thermal hyperalgesia, while the Y1 agonist, [Leu31, Pro34]NPY relieved thermal hyperalgesia. Mechanical and thermal hyperalgesia were both relieved by α-trinositol (PP56), a non-competitive antagonist of the actions of neuropeptide Y. Hyperalgesia was also relieved by surgical sympathectomy, which eliminated the effects of NPY and its agonists. These results suggest that neuropeptide Y contributes to peripheral hyperalgesia by actions at Y2 receptors, which may be located on postganglionic sympathetic terminals.
Elsevier