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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Specific involvement of PKC-epsilon in sensitization of the neuronal response to painful heat.

Pain is unique among sensations in that the perceived intensity increases, or sensitizes, during exposure to a strong stimulus. One important mediator of sensitization is bradykinin (BK), a peptide released as a consequence of tissue damage. BK enhances the membrane ionic current activated by heat in nociceptive neurons, using a pathway that involves activation of protein kinase C ( PKC). We find that five PKC isoforms are present in sensory neurons but that only PKC-epsilon is translocated to the cell membrane by BK. The heat response is sensitized when constitutively active PKC-epsilon is incorporated into nociceptive neurons. Conversely, BK-induced sensitization is suppressed by a specific peptide inhibitor of PKC-epsilon. We conclude that PKC-epsilon is principally responsible for sensitization of the heat response in nociceptors by bradykinin.[1]

References

  1. Specific involvement of PKC-epsilon in sensitization of the neuronal response to painful heat. Cesare, P., Dekker, L.V., Sardini, A., Parker, P.J., McNaughton, P.A. Neuron (1999) [Pubmed]
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