Antihyperalgesic effects of intrathecal neuropeptide Y during inflammation are mediated by Y1 receptors

  title={Antihyperalgesic effects of intrathecal neuropeptide Y during inflammation are mediated by Y1 receptors},
  author={Oludare B. Taiwo and Bradley K. Taylor},

Anti-nociceptive role of neuropeptide Y in the nucleus accumbens in rats with inflammation, an effect modulated by mu- and kappa-opioid receptors

Investigation of the effect of NPY in nociceptive modulation in the NAc of rats with inflammation, and the possible interation between NPY and the opioid systems suggests an involvement of antagonized the increased HWLs induced by preceding intra-NAc administration of the opioid antagonist nalozone.

Involvement of Neuropeptide Y in Post-Incisional Nociception in Rats

NPY is extensively expressed in the superficial laminae of the spinal cord and exhibit marked changes after incision, which indicates it is likely involved in post-incisional nociception.

Tonic inhibition of chronic pain by neuropeptide Y

Spinal NPY receptor systems are established as an endogenous braking mechanism that exerts a tonic, long-lasting, broad-spectrum inhibitory control of spinal nociceptive transmission, thus impeding the transition from acute to chronic pain.



Reduced antinociception and plasma extravasation in mice lacking a neuropeptide Y receptor

It is concluded that the Y1 receptor is required for central physiological and pharmacological NPY-induced analgesia and that its activation is both sufficient and required for the release of substance P and initiation of neurogenic inflammation.

Neuropeptide Y—Mediated Constriction and Dilation in Rat Middle Cerebral Arteries

  • J. YouL. EdvinssonR. Bryan
  • Biology, Medicine
    Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
  • 2001
The hypothesis that NPY can either constrict or dilate rat middle cerebral arteries (MCAs) is tested and BIBP 3226 (Y1 selective antagonist) significantly attenuated the NPY-and [Leu31, Pro34]-NPY–induced constrictions.

Characterization of the contractile effect of neuropeptide Y in feline cerebral arteries.

The data suggest that NPY mediates contraction of cerebrovascular smooth muscle via a mechanism that is dependent on the concentration of extracellular calcium.

Characterization of neuropeptide Y (NPY) receptors in human cerebral arteries with selective agonists and the new Y1 antagonist BIBP 3226

It is concluded that Y1 receptors exclusively, mediate the NPY‐induced contraction in human cerebral arteries and BIBP 3226 is a potent and competitive antagonist of this Y1‐mediated vasoconstriction.

Some sensory neurons express neuropeptide Y receptors: potential paracrine inhibition of primary afferent nociceptors following peripheral nerve injury

  • P. MantyhC. Allen S. Vigna
  • Biology
    The Journal of neuroscience : the official journal of the Society for Neuroscience
  • 1994
NPY receptors are uniquely positioned to inhibit primary afferent nociceptors directly, especially after peripheral nerve injury, previous studies have demonstrated.

Expression of neuropeptide Y and neuropeptide Y (Y1) receptor mRNA in rat spinal cord and dorsal root ganglia following peripheral tissue inflammation

The distinct upregulation of NPY and NPY (Y1) receptor in response to peripheral inflammation suggests an involvement ofNPY in the response to inflammation and in nociception.