Primary afferent tachykinins are required to experience moderate to intense pain

Yu Qing Cao, Patrick W. Mantyh, Elaine J. Carlson, Anne-Marie Gillespie, Charles J. Epstein and Allan I. Basbaum ()
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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

Nature, 1998, vol. 392, issue 6674, 390-394

Abstract: 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.

Date: 1998
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DOI: 10.1038/32897

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