Mechanisms involved in the nociception produced by peripheral protein kinase c activation in mice

  title={Mechanisms involved in the nociception produced by peripheral protein kinase c activation in mice},
  author={Juliano Ferreira and Karen M. Trich{\^e}s and Rodrigo Medeiros and Jo{\~a}o B. Calixto},

Phosphorylation of TRPV1 S801 Contributes to Modality-Specific Hyperalgesia in Mice

In vivo evidence is provided for a highly specific inhibition that leaves basal TRPV1 function intact, yet alleviates some forms of hyperalgesia, and supports inhibition of TRpV1 S801 phosphorylation as a potential intervention for pain management.

Effect of PKC/NF-κB on the Regulation of P2X3 Receptor in Dorsal Root Ganglion in Rats with Sciatic Nerve Injury

The upregulation of p-PKCα, p-NF-κB p65, and P2X3R expression in the DRGs of CCI rats was involved in the occurrence and development of neuropathic pain.

Mechanisms involved in IL-6-induced muscular mechanical hyperalgesia in mice

Phosphoinositide 3-Kinase Binds to TRPV1 and Mediates NGF-stimulated TRPV1 Trafficking to the Plasma Membrane

A new model for NGF-mediated hyperalgesia is proposed in which physical coupling of TRPV1 and PI3K in a signal transduction complex facilitates trafficking of TRpV1 to the plasma membrane.

Possible participation of nitric oxide/cyclic guanosine monophosphate/protein kinase C/ATP-sensitive K(+) channels pathway in the systemic antinociception of flavokawin B.

Data indicate that the NO/cyclic guanosine monophosphate/PKC/ATP-sensitive K(+) channel pathway possibly participated in the antinociceptive action induced by FKB.

Potentiation of transient receptor potential V1 functions by the activation of metabotropic 5‐HT receptors in rat primary sensory neurons

Results suggest that the PKC‐ and PKA‐mediated signalling pathways are involved in the potentiating effect of 5‐HT on TRPV1 functions through the activation of5‐HT2A and 5‐ HT7 receptors, respectively.



In vivo evidence for a role of protein kinase C in peripheral nociceptive processing

It is demonstrated that PKC activation at peripheral tissues leads to the development of spontaneous nociceptive response, thermal hyperalgesia and mechanical allodynia, and in vivo evidence that peripheral PKCactivation is essential for the full establishment of the nocICEptive response induced by two different inflammatory stimuli.

A novel nociceptor signaling pathway revealed in protein kinase C epsilon mutant mice.

It is shown that epinephrine-induced mechanical and thermal hyperalgesia and acetic acid-associated hyperalGESia are markedly attenuated in PKCepsilon mutant mice, but baseline nociceptor thresholds are normal, indicating that PKCEPsilon regulates nocICEptor function and suggesting thatPKCep silon inhibitors could prove useful in the treatment of pain.

Chronic hypersensitivity for inflammatory nociceptor sensitization mediated by the epsilon isozyme of protein kinase C.

The findings indicate that different second messenger pathways underlie acute and prolonged inflammatory pain, which may have a role in chronic inflammatory pain.

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

KC-epsilon is principally responsible for sensitization of the heat response in nociceptors by bradykinin, a peptide released as a consequence of tissue damage.

Bradykinin‐induced activation of nociceptors: receptor and mechanistic studies on the neonatal rat spinal cord‐tail preparation in vitro

The data show that bradykinin produces concentration‐dependent activation of peripheral nociceptors in the neonatal rat tail and responses were unaffected by calcium channel block and were partially dependent on the production of prostanoids.

Phosphatidylinositol 3-Kinase Activates ERK in Primary Sensory Neurons and Mediates Inflammatory Heat Hyperalgesia through TRPV1 Sensitization

PI3K induces heat hyperalgesia, possibly by regulating TRPV1 activity, in an ERK-dependent manner, and appears to play a role that is distinct from ERK by regulating the early onset of inflammatory pain.

Protein kinase C activation potentiates gating of the vanilloid receptor VR1 by capsaicin, protons, heat and anandamide

The absence of a current activated by PMA in most DRG neurones or in stably transfected HEK293 cells suggests that activation of PKC does not directly open VR1 channels, but instead increases the probability that they will be activated by capsaicin, heat, low pH or anandamide.