Aim:To explore the modulatory effect of bradykinin (BK) on 5-HT_3 receptor-mediated current in trigeminal ganglion (TG) neurons in rats.Methods:The whole-cell patch-clamp technique was used to record 5-HT-activated currents (I_(5-HT)) inneurons freshly dissociated from rat TG.Drugs were applied by rapid solutionexchange.Results:The majority of the neurons examined responded to 5-HTapplied externally with an inward current (76.3%,74/97) that could be blocked bythe 5-HT_3 receptor antagonist,ICS-205,930 (1×10~(-6) mol/L).In 66 of the 74 cellssensitive to 5-HT (89.2%),pretreatment for 30 s with BK (1×10~(-6)-1×10~(-10) mol/L)could potentiate I_(5-HT) with the maximal modulatory effect occurring at10~(-7) mol/L BK (71.6%+4.9%).BK shifted the 5-HT concentration-response curveupwards with an increase of 68.9%±7.2% in the maximal current response,but withno significant change in the EC_(50) value (19.1±3.2 μmol/L vs 20.9±3.5 μmol/L;t-test,P>0.05;n=8).BK potentiated I_(5-HT) in a holding potential-independent manner anddid not alter the reverse potential of I_(5-HT).This BK-induced potentiation ofI_(5-HT) was almost completely blocked by Hoe 140 (5×10~(-7) mol/L),a selective B_2 BKreceptor 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 I_(5-HT) via a PKC-dependent pathway in rat TG neurons,which may explain the peripheral’mecha-nism of pain and hyperalgesia caused by,for example,tissue damage andinflammation. Aim: To explore the modulatory effect of bradykinin (BK) on 5-HT_3 receptor-mediated current in trigeminal ganglion (TG) neurons in rats. Methods: The whole-cell patch-clamp technique was used to record 5-HT-activated currents (I_ (5-HT)) inneurons freshly dissociated from rat TG. Drugs were applied by rapid solution exchange. Results: The majority of the neurons examined responded to 5-HTapplied externally with an inward current (76.3%, 74/97) be blocked by the 5-HT_3 receptor antagonist, ICS-205,930 (1 × 10 -6 mol / L) .In 66 of the 74 cellssensitive to 5-HT 10 -6 -6 × -1 10 -10 mol / L could potentiate I_ (5-HT) with the maximal modulatory effect occurring at10 ~ (-7) mol / L BK (71.6% + 4.9%) .BK shifted the 5-HT concentration-response curveupwards with an increase of 68.9% ± 7.2% in the maximal current response, but with no significant change in the EC 50 value (19.1 ± 3.2 μmol / L vs. 20.9 ± 3.5 μmol / L; t-test, P> 0.05; n = 8) .BK potentiated I_ (5-HT) in a holdi ng potential-independent manner and do not alter the reverse potential of I_ (5-HT). This BK-induced potentiation of I_ (5-HT) was almost completely blocked by Hoe 140 (5 × 10 -7 mol / L) , a selective B_2 BKreceptor 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. Confclusion: Pre- application of BK exerts an enhancing effect on I_ (5-HT) via a PKC-dependent pathway in rat TG neurons, which may explain the peripheral’mecha-nism of pain and hyperalgesia caused by, for example, tissue damage and inflamation.