〔Abstract〕 Objective To study the effects of dexmedetomidine(DEX) on the excitability of locus coeruleus(LC) neurons in the brain stem in order to elucidate the central mechanisms of the analgesic effects of DEX. Methods The effects of DEX on the mechanical and thermal pain thresholds in adult male C57 BL/6 mice were examined and the sedative behavior scores were evaluated. The effects of DEX on the discharge of LC neurons in free moving mice were measured by multichannel electrophysiologyin vivo. The analgesic and sedative effects of DEX were detected by behavioral tests with intrathecal injection of α2receptor antagonists or morphine receptor antagonists. Results Dex in high dose(12～20 μg/kg) intraperitoneal injected could increase the thresholds of mechanical and thermal pain in mice and they showed significant sedation. Both the sedative and analgesic effects of DEX were dose-dependent. Multichannel electrophysiological recordingsin vivoshowed that the discharge frequencies of LC neurons were increased by DEX in low dose, while they were decreased by DEX in high dose. Intrathecal injection of yohimbine, an α2receptor antagonist, significantly inhibited the analgesic effect of DEX in low dose, but did not affect the sedative effect of DEX in high dose. Intrathecal injection of naloxone, a morphine receptor antagonist, did not affect the analgesic effect of DEX. Conclusion DEX exerts analgesic effects by activating the descending inhibition system of LC, and the spinal α2receptor involves in analgesic effects of DEX. Nevertheless, the sedative effects of DEX are not mediated by the descending inhibition system from LC to spinal cord.