@article{APS3583,
author = {Wang-ping HU and Xue-mei LI and Ji-liang WU and Min ZHENG and Zhi-wang LI},
title = {Bradykinin potentiates 5-HT 3 receptor-mediated current in rat trigeminal ganglion neurons},
journal = {Acta Pharmacologica Sinica},
volume = {26},
number = {4},
year = {2016},
keywords = {},
abstract = {Aim: To explore the modulatory effect of bradykinin (BK) on 5-HT3 receptormediated
current in trigeminal ganglion (TG) neurons in rats. Methods: The wholecell
patch-clamp technique was used to record 5-HT-activated currents (I5-HT) in
neurons freshly dissociated from rat TG. Drugs were applied by rapid solution
exchange. Results: The majority of the neurons examined responded to 5-HT
applied externally with an inward current (76.3%, 74/97) that could be blocked by
the 5-HT3 receptor antagonist, ICS-205,930 (1×10-6 mol/L). In 66 of the 74 cells
sensitive to 5-HT (89.2%), pretreatment for 30 s with BK (1×10-6–1×10-10mol/L)
could potentiate I5-HT with the maximal modulatory effect occurring at
10-7mol/L BK (71.6%±4.9%). BK shifted the 5-HT concentration-response curve
upwards with an increase of 68.9%±7.2% in the maximal current response, but with
no significant change in the EC50 value (19.1±3.2 μmol/L vs 20.9±3.5 μmol/L; t-test,
P0.05; n=8). BK potentiated I5-HT in a holding potential-independent manner and
did not alter the reverse potential of I5-HT. This BK-induced potentiation of
I5-HTwas almost completely blocked by Hoe 140 (5×10-7 mol/L), a selective B2 BK
receptor antagonist, and was removed after intracellular dialysis of GF-109203X
(2 μmol/L), a selective protein kinase C (PKC) inhibitor, with the re-patch clamp.
Conclusion: Pre-application of BK exerts an enhancing effect on I5-HT via a PKCdependent
pathway in rat TG neurons, which may explain the peripheral mechanism
of pain and hyperalgesia caused by, for example, tissue damage and
inflammation.},
issn = {1745-7254}, url = {http://www.chinaphar.com/article/view/3583}
}