Mechanisms involved in an increment of multimodal excitability of medullary and upper cervical dorsal horn neurons following cutaneous capsaicin treatment

doi:10.1186/1744-8069-4-59

Molecular Pain

Volume 4

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Honda K
Kitagawa J
Sessle BJ
Kondo M
Tsuboi Y
Yonehara Y
Iwata K

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Kitagawa J
Sessle BJ
Kondo M
Tsuboi Y
Yonehara Y
Iwata K
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Mechanisms involved in an increment of multimodal excitability of medullary and upper cervical dorsal horn neurons following cutaneous capsaicin treatment

Kuniya Honda¹ , Junichi Kitagawa²^,4 , Barry J Sessle³ , Masahiro Kondo²^,4 , Yoshiyuki Tsuboi²^,4 , Yoshiyuki Yonehara¹ and Koichi Iwata²^,4^,5

¹Department of Oral and Maxillofacial Surgery, Nihon University School of Dentistry, 1-8-13 Kandasurugadai, Chiyoda-ku Tokyo, 101-8310, Japan

²Department of Physiology, Nihon University School of Dentistry, 1-8-13 Kandasurugadai, Chiyoda-ku Tokyo, 101-8310, Japan

³Department of Oral Physiology, Faculty of Dentistry, University of Toronto, 124 Edward Street, Toronto, Ontario M5G 1G6, Canada

⁴Division of Functional Morphology, Dental Research Center, Nihon University School of Dentistry, Tokyo 101-8310, Japan

⁵Division of Applied System Neuroscience Advanced Medical Research Center, Nihon University Graduate School of Medical Science, 30-1 Ohyaguchi-Kamimachi Itabashi, Tokyo 173-8610, Japan

author email corresponding author email

Molecular Pain 2008, 4:59doi:10.1186/1744-8069-4-59


Published:	19 November 2008

Abstract

Background

In order to evaluate mechanisms that may underlie the sensitization of trigeminal spinal subnucleus caudalis (Vc; the medullary dorsal horn) and upper cervical spinal cord (C1-C2) nociceptive neurons to heat, cold and mechanical stimuli following topical capsaicin treatment of the facial skin, nocifensive behaviors as well as phosphorylation of extracellular regulated-kinase (pERK) in Vc and C1-C2 neurons were studied in rats.

Results

Compared to vehicle application, capsaicin application to the lateral facial skin produced 1 hour later a flare in the skin, and also induced significantly greater nocifensive behaviors to heat, cold or mechanical stimulus of the lateral facial skin. The intrathecal (i.t.) injection of the MEK inhibitor PD98059 markedly attenuated the nocifensive behaviors to these stimuli in capsaicin-treated rats. Moreover, the number of pERK-like immunoreactive (pERK-LI) cells in Vc and C1-C2 was significantly larger following the heat, cold and mechanical stimuli in capsaicin-treated rats compared with vehicle-treated rats. The number of pERK-LI cells gradually increased following progressive increases in the heat or mechanical stimulus intensity and following progressive decrease in the cold stimulus. The ERK phosphorylation in Vc and C1-C2 neurons was strongly inhibited after subcutaneous injection of the capsaicin antagonist capsazepine in capsaicin-treated rats.

Conclusion

The present findings revealed that capsaicin treatment of the lateral facial skin causes an enhancement of ERK phosphorylation in Vc and C1-C2 neurons as well as induces nocifensive behavior to heat, cold and mechanical simulation of the capsaicin-treated skin. The findings suggest that TRPV1 receptor mechanisms in rat facial skin influence nociceptive responses to noxious cutaneous thermal and mechanical stimuli by inducing neuroplastic changes in Vc and C1-C2 neurons that involve in the MAP kinase cascade.