中文摘要：

目的：探索杏仁中央核在抑郁导致的痛觉减退中的作用.方法：采用慢性不确定温和应激（unpredictable chronic mild stress,UCMS）在大鼠身上建立抑郁模型,50只雄性wistar大鼠随机分为正常/盐水、正常/蝇蕈醇（muscimol）、UCMS/盐水和UCMS/muscimol 4组.建模成功后根据分组在杏仁中央核内注射muscimol或盐水,用糖水偏好和辐射热痛阈分别测抑郁和诱发痛.结果：6周慢性应激处理后,UCMS组大鼠与对照组相比糖水偏好下降（P＜0.001）,痛阈增加（P＜0.001）.与盐水对照相比,控制组大鼠双侧杏仁中央核注射muscimol后糖水偏好没有改变,痛阈增加（P＜0.001）;而UCMS组大鼠糖水偏好增加（P＜0.05）,痛阈降低（P＜0.05）.结论：抑制UCMS抑郁样大鼠杏仁中央核的活动可以缓解抑郁以及抑郁引起的痛觉减退.杏仁中央核活动异常增加是抑郁引起痛觉减退的重要原因.

英文摘要：

Objective：To investigate the role of central amygdala in depression-induced hypoalgesia.Methods：The study adopted unpredictable chronic mild stress （UCMS） model in rats to simulate clinical depression.A total of 50 male wistar rats were randomly divided into 4 groups：control/saline,control/muscimol,UCMS/saline and UCMS/muscimol.After the depression model was established,GABAA receptor agonist muscimol or normal saline was micminjected into the central amygdala,sucrose preference test and radiant heat pain threshold test were used to measure the depressive-like behavior and nociceptive response respectively.Results：After a 6-weeks period of stress exposure,the UCMS-treated rats showed significantly decreased sucrose preference （P ＜ 0.001） and increased radiant heat pain threshold （P ＜ 0.001） as compared with the rats in control group.Additionally,bilateral microinjection of muscimol into central amygdala did not affect the amount of sucrose intake but increased radiant heat pain threshold in the control rats （P ＜ 0.001）.Moreover,microinjection ofmuscimol into central amygdala increased the sucrose preference （P ＜ 0.05） and decreased the radiant heat pain threshold in the UCMS-treated rats （P ＜ 0.05）.Conclusion：Inhibition the activity of central amygdala can reduce depressive-like behaviors and associated hypoalgesia in UCMS-exposed rats.Abnormal hyperactivity of central amygdala may play an important role in depression-induced hypoalgesia.