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

Philippe Naveilhan, Hessameh Hassani, Guilherme Lucas, Karin Hygge Blakeman, Jing-Xia Hao, Xiao-Jun Xu, Zsuzsanna Wiesenfeld-Hallin, Peter Thorén and Patrik Ernfors ()
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Philippe Naveilhan: and
Hessameh Hassani: and
Guilherme Lucas: and
Karin Hygge Blakeman: Huddinge University Hospital, Karolinska Institute
Jing-Xia Hao: Huddinge University Hospital, Karolinska Institute
Xiao-Jun Xu: Huddinge University Hospital, Karolinska Institute
Zsuzsanna Wiesenfeld-Hallin: Huddinge University Hospital, Karolinska Institute
Peter Thorén: Karolinska Institute
Patrik Ernfors: and

Nature, 2001, vol. 409, issue 6819, 513-517

Abstract: Abstract Neuropeptide Y (NPY) is believed to exert antinociceptive actions by inhibiting the release of substance P and other ‘pain neurotransmitters’ in the spinal cord dorsal horn1,2,3. However, the physiological significance and potential therapeutic value of NPY remain obscure4. It is also unclear which receptor subtype(s) are involved. To identify a possible physiological role for the NPY Y1 receptor in pain transmission, we generated NPY Y1 receptor null mutant (Y1-/-) mice by homologous recombination techniques. Here we show that Y1-/- mice develop hyperalgesia to acute thermal, cutaneous and visceral chemical pain, and exhibit mechanical hypersensitivity. Neuropathic pain is increased, and the mice show a complete absence of the pharmacological analgesic effects of NPY. In the periphery, Y1 receptor activation is sufficient and required for substance P release and the subsequent development of neurogenic inflammation and plasma leakage. We conclude 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.

Date: 2001
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DOI: 10.1038/35054063

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