Neuropathic pain remains a significant clinical problem and is often resistant to conventional analgesics.Large conductance calcium-activated potassium (MaxiK/BKca) channels are expressed in many different types of neurons and are involved in the regulation of neuronal excitability and function.Peripheral nerve injury causes plasticity of primary and secondary afferent neurons, leading to central sensitization and neuropathie pain.The aim of this study was to investigate the possible involvment of BKca channels in the molecular mechanisms underlying the increased excitability of neurons in the rat trigeminal ganglion (TG) and trigeminal nucleus caudalis (TNC)after chronic constriction injury of the infraorbital branch of the trigeminal nerve (ION-CCI).Nociceptive testing, real-time quantitative reverse transcription-polymerase chain reaction analysis (QT-RT-PCR), western blot methods and whole-cell patch clamp recording were used to investigate the role of BKca channels in the trigeminal neuropathic pain.Rats produced significant mechanical allodynia in the whisker pad of the operated side from 6 d to 42 d after ION-CCl.BKca channel agonist NS1619 (20-100 μg) significantly and dose-dependently attenuated the facial mechanical allodynia and increased the facial mechanical pain threshold in ION-CCI rats 15 d after operation.