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Primary afferent tachykinins are required to experience moderate to intense pain

Author

Listed:
  • Yu Qing Cao

    (Physiology and W. M. Keck Foundation Center for Integrative Neuroscience)

  • Patrick W. Mantyh

    (Molecular Neurobiology Laboratory, University of Minnesota)

  • Elaine J. Carlson

    (University of California San Francisco)

  • Anne-Marie Gillespie

    (University of California San Francisco)

  • Charles J. Epstein

    (University of California San Francisco)

  • Allan I. Basbaum

    (Physiology and W. M. Keck Foundation Center for Integrative Neuroscience)

Abstract

The excitatory neurotransmitter glutamate coexists with the peptide known as substance P in primary afferents that respond to painful stimulation1. Because blockers of glutamate receptors reliably reduce pain behaviour2,3,4, it is assumed that ‘pain’ messages are mediated by glutamate action on dorsal horn neurons. The contribution of substance P, however, is still unclear. We have now disrupted the mouse preprotachykinin A gene (PPT-A), which encodes substance P and a related tachykinin, neurokinin A (ref. 5). We find that although the behavioural response to mildly painful stimuli is intact in these mice, the response to moderate to intense pain is significantly reduced. Neurogenic inflammation, which results from peripheral release of substance P and neurokinin A (ref. 6), is almost absent in the mutant mice. We conclude that the release of tachykinins from primary afferent pain-sensing receptors (nociceptors) is required to produce moderate to intense pain.

Suggested Citation

  • Yu Qing Cao & Patrick W. Mantyh & Elaine J. Carlson & Anne-Marie Gillespie & Charles J. Epstein & Allan I. Basbaum, 1998. "Primary afferent tachykinins are required to experience moderate to intense pain," Nature, Nature, vol. 392(6674), pages 390-394, March.
    • Handle: RePEc:nat:nature:v:392:y:1998:i:6674:d:10.1038_32897
    DOI: 10.1038/32897
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