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Journal of Dental Research
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Biological

Time-dependent Activation of ERK1/2 in Nerve Terminals of the Dentin-Pulp Complex following Bradykinin Treatment

Y. Korkmaz1,*, W. Bloch2, K. Schneider1, S. Zimmer3, K. Addicks4 and W.H.-M. Raab1

1 Dept. of Operative and Preventive Dentistry and Endodontics, Heinrich-Heine-University, Moorenstrasse 5, 40225 Düsseldorf, Germany;
2 Dept. of Molecular and Cellular Sports Medicine, German Sports University, Cologne, Germany;
3 Dept. of Operative Dentistry, University Witten/Herdecke, Witten, Germany; and
4 Dept. I of Anatomy, University of Cologne, Germany

Correspondence: * corresponding author, yueksel.korkmaz{at}uni-duesseldorf.de

The extracellular signal-regulated kinases 1 and 2 (ERK1/2) have been implicated in the inflammation-dependent sensitization of nociceptors, and the inflammatory mediator bradykinin (BK) led to a reduced threshold in the nociceptor terminals, activating intracellular signaling by phosphorylating receptors and ion channels. The effects of BK on the non-transcriptional modulation of the ERK1/2 in the peripheral nociceptor terminals, including in nerve endings of the dentin-pulp complex, are unknown. The time-dependent effects of BK (10–7 M) on the ERK1/2 phosphorylation in nerve terminals of the dentin-pulp complex were investigated by quantitative and double immunolabeling with organ bath experiments. In nerve terminals, total and p-ERK1/2 were detected. In comparison with the controls, the numbers of p-ERK1/2-positive nerve endings increased after 1 and 3 min and decreased after 10 min of BK treatment. Analysis of the data indicates that BK induces phosphorylation-mediated local activation of ERK1/2 in nerve terminals modulating nociception in the dentin-pulp complex.

Key Words: mitogen-activated protein kinase (MAPK) • extracellular signal-regulated protein kinase 1/2 (ERK1/2) • bradykinin • peripheral sensitization • dentin nociception

Journal of Dental Research, Vol. 87, No. 12, 1149-1154 (2008)
DOI: 10.1177/154405910808701202
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