Facial pain induces the alteration of transient receptor potential vanilloid receptor 1 expression in rat trigeminal ganglion

被引:27
作者
Pei L. [1 ]
Lin C.-Y. [1 ]
Dai J.-P. [1 ]
Yin G.-F. [1 ]
机构
[1] Department of Neurobiology, Tongji Medical College, Huazhong University of Science and Technology
关键词
Facial pain; Hyperalgesia; Trigeminal ganglion; Vanilloid receptors;
D O I
10.1007/s12264-007-0013-2
中图分类号
学科分类号
摘要
Objective: To investigate the involvement of transient receptor potential vanilloid receptor 1 (TRPV1) in the facial inflammatory pain in relation to thermal hyperalgesia and cold pain sensation. Methods: Facial inflammatory pain model was developed by subcutaneous injection of turpentine oil (TO) into rat facial area. Head withdrawal thermal latency (HWTL) and head withdrawal cold latency (HWCL) were measured once a day for 21 d after TO treatment using thermal and cold measurement apparatus. The immunohistochemical staining, cell-size frequency analysis and the survey of average optical density (OD) value were used to observe the changes of TRPV1 expression in the neurons of the trigeminal ganglion (TG), peripheral nerve fibers in the vibrissal pad, and central projection processes in the trigeminal sensory nuclei caudalis (Vc) on day 3, 5, 7, 14, and 21 after TO injection. Results: HWTL and HWCL decreased significantly from day 1 to day 14 after TO injection with the lowest value on day 5 and day 3, respectively, and both recovered on day 21. The number of TRPV1-labeled neurons increased remarkably from day 1 to day 14 with a peak on day 7, and returned back to the normal level on day 21. In control rats, only small and medium-sized TG neurons were immunoreactive (IR) to TRPV1, and the TRPV1-IR terminals were abundant in both the vibrissal pad and the Vc. Within 2 weeks of inflammation, the expression of TRPV1 in small and medium-sized TG neurons increased obviously. Also the TRPV1 stained terminals and fibers appeared more frequent and denser in both the vibrissal pad skin and throughout laminae I and the outer zone of laminae II (IIo) of Vc. Conclusion: Facial inflammatory pain could induce hyperalgesia to noxious heat and cold stimuli, and result in increase of the numbers of TRPV1 positive TG neurons and the peripheral and central terminals of TG. These results suggest that the phenotypic changes of TRPV1 expression in small and medium-sized TG neurons and terminals might play an important role in the development and maintenance of TO-induced inflammatory thermal hyperalgesia and cold pain sensation.
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页码:92 / 100
页数:8
相关论文
共 22 条
[1]  
Caterina M.J., Julius D., The vanilloid receptor: A molecular gateway to the pain pathway, Annu Rev Neurosci, 24, pp. 487-517, (2001)
[2]  
Tominaga M., Julins D., Capsaicin receptor in the pain pathway, Jpn J Pharmacol, 83, pp. 20-24, (2000)
[3]  
Guo A., Vulchanova L., Wang J., Li X., Eide R., Immunocytochemical localization of the vanilloid receptor 1 (VR1): Relation to neuropeptides, the P2X3 purinoceptor and IB4 binding sites, Eur J Neurosci, 11, pp. 946-958, (1999)
[4]  
Carlton S.M., Coggeshall R.E., Peripheral capsaicin receptors increase in the inflamed rat hindpaw: A possible mechanism for peripheral sensitization, Neurosci Lett, 310, pp. 53-56, (2001)
[5]  
Caterina M.J., Leffler A., Malmberg A.B., Martin W.J., Trafton J., Petersen-Zeitz K.R., Et al., Impaired nociception and pain sensation in mice lacking the capsaicin receptor, Science, 288, pp. 306-313, (2000)
[6]  
Amaya F., Oh-hashi K., Naruse Y., Iijima N., Ueda M., Shimosato G., Et al., Local inflammation increases vanilloid receptor 1 expression within distinct subgroups of DRG neurons, Brain Res, 963, pp. 190-196, (2003)
[7]  
Zhou Y., Li G.D., Zhao Z.Q., State-dependent phosphorylation of epsilon-isozyme of protein kinase C in adult rat dorsal root ganglia after inflammation and nerve injury, J Neurochem, 85, pp. 571-580, (2003)
[8]  
Ji R., Samad T., Jin S., Schmoll R., Woolf C., p38 MAPK activation by NGF in primary sensory neurons after inflammation increases TRPV1 levels and maintains heat hyperalgesia, Neuron, 36, pp. 57-68, (2002)
[9]  
Tominaga M., Wada M., Masu M., Potentiation of capsaicin receptor activity by metabotropic ATP receptors as a possible mechanism for ATP-evoked pain and hyperalgesia, Proc Natl Acad Sci USA, 98, pp. 6951-6956, (2001)
[10]  
Premkumar L.S., Ahern G.P., Induction of vanilloid receptor channel activity by protein kinase C, Nature, 408, pp. 985-990, (2000)