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. 1999 Jul;23(3):617-24.
doi: 10.1016/s0896-6273(00)80813-2.

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

P Cesare  1 , L V Dekker, A Sardini, P J Parker, P A McNaughton
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Free article

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

P Cesare et al. Neuron. 1999 Jul.
Free article

Abstract

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.

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