CELLULAR, MOLECULAR AND DEVELOPMENTAL NEUROSCIENCEAcute PAR2 activation reduces α, β-MeATP sensitive currents in rat dorsal root ganglion neuronsLu, Zhi-Jiea; Miao, Xue-Ronga; Wu, Jing-Xianga; Wang, Xiao-Yanb; Miao, Qinga; Yu, Wei-FengaAuthor Information aDepartment of Anesthesiology, Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, Shanghai bDepartment of Anesthesiology, First Affiliated Hospital to PLA General Hospital, Beijing, China Correspondence to Dr Wei-Feng Yu, Department of Anesthesiology, Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, 225 Changhai Road, Shanghai 200438, China Tel: +86 212181875231; fax: +86 212181875231; e-mail: firstname.lastname@example.orgZhi-Jie Lu and Xue-Rong Miao contributed equally to this research work Received 13 December 2009 accepted 16 December 2009 NeuroReport: February 17th, 2010 - Volume 21 - Issue 3 - p 227-232 doi: 10.1097/WNR.0b013e328336b6c8 Buy Metrics Abstract It has been reported that proteinase-activated receptor 2 (PAR2) receptor activation enhances the animal's pain response and PAR2 coexpresses with P2X3 in dorsal root ganglion neurons. However, whether PAR2 activation has a direct impact on P2X3 currents is still not clear. In this study, we performed the patch-clamp experiments in cultured dorsal root ganglion neurons and found that when incubated with trypsin or the PAR2 agonist SL-NH2 for a short time (3 min), instead of increasing, P2X3 currents amplitude decreased significantly. Meanwhile, the opening of P2X3 ion channel accelerated. Protein kinase A inhibitor H89 could not reverse above phenomenon, but played a synergistic effect on the contrary. These results suggest that the enhanced pain response caused by PAR2 activation is not through direct increase of the P2X3 current amplitude, and the acceleration of P2X3 opening may participate in the enhanced pain response in a long-time view. Moreover, protein kinase A does not participate in the inhibition of P2X3 currents caused by PAR2 activation. © 2010 Lippincott Williams & Wilkins, Inc.