A pro-nociceptive role of neuromedin U in adult mice

Pain. 2003 Aug;104(3):609-616. doi: 10.1016/S0304-3959(03)00118-0.


Although the neuropeptide neuromedin U (NMU) was first isolated from the spinal cord, its actions in this site are unknown. The recent identification of the NMU receptor subtype 2 (NMU2R) in the spinal cord has increased the interest in investigating the role of NMU in this part of the central nervous system. Here, we report a novel function for NMU in spinal nociception in the mouse. Systemic perfusion of NMU (rat, NMU-23) dose-dependently (0.2, 0.5, 1, and 2.5 microM) potentiated both the background activity and noxious pinch-evoked response of nociceptive or wide dynamic range, but not non-nociceptive, dorsal horn neurons. At 2.5 microM, NMU-23 increased the total background activity from 154+/-34 to 1374+/-260 spikes/160 s (P<0.005, n=28) and increased the evoked nociceptive response by 185+/-50% (P<0.01, n=13). Intrathecal administration of NMU-23 (0.4, 1.1, and 3.8 nmol/10 microl) dose-dependently decreased thermal withdrawal latencies and produced a morphine-sensitive behavioral response. These electrophysiological and behavioral results suggest that NMU may be a novel physiological regulator in spinal nociceptive transmission and processing.

Publication types

  • Comparative Study

MeSH terms

  • Action Potentials / drug effects
  • Action Potentials / physiology
  • Animals
  • Dose-Response Relationship, Drug
  • Male
  • Membrane Proteins*
  • Mice
  • Neuropeptides / toxicity*
  • Pain / chemically induced*
  • Pain / physiopathology
  • Pain Measurement / drug effects*
  • Pain Measurement / methods
  • Posterior Horn Cells / drug effects
  • Posterior Horn Cells / physiology
  • Rats
  • Receptors, Neurotransmitter / agonists
  • Receptors, Neurotransmitter / physiology


  • Membrane Proteins
  • Neuropeptides
  • Receptors, Neurotransmitter
  • neuromedin U receptor
  • neuromedin U