Altered nociception, analgesia and aggression in mice lacking the receptor for substance P

Carmen De Felipe, Juan F. Herrero, John A. O'Brien, James A. Palmer, Christopher A. Doyle, Andrew J. H. Smith, Jennifer M. A. Laird, Carlos Belmonte, Fernando Cervero and Stephen P. Hunt ()
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Carmen De Felipe: Instituto de Neurociencias, Universidad Miguel Hernandez
Juan F. Herrero: Universidad de Alcala, Facultad de Medicina, Campus Universitario
John A. O'Brien: MRC Laboratory of Molecular Biology
James A. Palmer: MRC Laboratory of Molecular Biology
Christopher A. Doyle: MRC Laboratory of Molecular Biology
Andrew J. H. Smith: Centre for Genome Research, University of Edinburgh, King's Buildings
Jennifer M. A. Laird: Universidad de Alcala, Facultad de Medicina, Campus Universitario
Carlos Belmonte: Instituto de Neurociencias, Universidad Miguel Hernandez
Fernando Cervero: Universidad de Alcala, Facultad de Medicina, Campus Universitario
Stephen P. Hunt: MRC Laboratory of Molecular Biology

Nature, 1998, vol. 392, issue 6674, 394-397

Abstract: Abstract The peptide neurotransmitter substance P modulates sensitivity to pain by activating the neurokinin-1 (NK-1) receptor, which is expressed by discrete populations of neurons throughout the central nervous system1,2,3,4. Substance P is synthesized by small-diameter sensory ‘pain’ fibres5, and release of the peptide into the dorsal horn of the spinal cord following intense peripheral stimulation6 promotes central hyperexcitability and increased sensitivity to pain7,8,9,10. However, despite the availability of specific NK-1 antagonists4, the function of substance P in the perception of pain remains unclear. Here we investigate the effect of disrupting the gene encoding the NK-1 receptor in mice. We found that the mutant mice were healthy and fertile, but the characteristic amplification (‘wind up’) and intensity coding of nociceptive reflexes was absent. Although substance P did not mediate the signalling of acute pain or hyperalgesia, it was essential for the full development of stress-induced analgesia and for an aggressive response to territorial challenge, demonstrating that the peptide plays an unexpected role in the adaptive response to stress.

Date: 1998
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DOI: 10.1038/32904

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