Chlorogenic acid(5-caffeoylquinic acid, CGA) is a phenolic compound that is found ubiquitously in plants, fruits and vegetables and is formed via the esterification of caffeic acid and quinic acid. In addition to its notable biological functions against cardiovascular diseases, type-2 diabetes and inflammatory conditions, CGA was recently hypothesized to be an alternative for the treatment of neurological diseases such as Alzheimer’s disease and neuropathic pain disorders. However, its mechanism of action is unclear.Voltage-gated potassium channel(Kv) is a crucial factor in the electro-physiological processes of sensory neurons. Kv has also been identified as a potential therapeutic target for inflammation and neuropathic pain disorders. In this study, we analysed the effects of CGA on the two main subtypes of Kv in trigeminal ganglion neurons, namely, the IK,Aand IK,Vchannels. Trigeminal ganglion(TRG)neurons were acutely disassociated from the rat TRG, and two different doses of CGA(0.2 and 1 mmol·L21) were applied to the cells.Whole-cell patch-clamp recordings were performed to observe alterations in the activation and inactivation properties of the IK,Aand IK,Vchannels. The results demonstrated that 0.2 mmol·L21CGA decreased the peak current density of IK,A. Both 0.2 mmol·L21and1 mmol·L21CGA also caused a significant reduction in the activation and inactivation thresholds of IK,Aand IK,V. CGA exhibited a strong effect on the activation and inactivation velocities of IK,Aand IK,V. These findings provide novel evidence explaining the biological effects of CGA, especially regarding its neurological effects. Chlorogenic acid (5-caffeoylquinic acid, CGA) is a phenolic compound that is found ubiquitously in plants, fruits and vegetables and is formed via the esterification of caffeic acid and quinic acid. In addition to its notable biological functions against cardiovascular diseases, type- 2 diabetes and inflammatory conditions, CGA was recently hypothesized to be an alternative for the treatment of neurological diseases such as Alzheimer’s disease and neuropathic pain disorders. However, its mechanism of action is unclear. Vitamin-gated potassium channel (Kv) is a crucial factor in the electro-physiological processes of sensory neurons. Kv has also been identified as a potential therapeutic target for inflammation and neuropathic pain disorders. In this study, we have analyzed the effects of CGA on the two main subtypes of Kv in trigeminal ganglion neurons, ie , the IK, A and IK, Vchannels. Trigeminal ganglion (TRG) neurons were acutely disassociated from the rat TRG, and two different doses of CGA (0 .2 and 1 mmol·L21) were applied to the cells. Whole-cell patch-clamp recordings were performed to observe alterations in the activation and inactivation properties of the IK, Aand IK, Vchannels. The results performance that 0.2 mmol·L21 CGA the peak current density of IK, A. Both 0.2 mmol·L21 and 1 mmol·L21 CGA also caused a significant reduction in the activation and inactivation thresholds of IK, Aand IK, V. CGA showed a strong effect on the activation and inactivation velocities of IK, Aand IK, V. These findings provide novel evidence explaining the biological effects of CGA, especially regarding its neurological effects.