Objective: To investigate the regulatory effect of blue light on the expression of brain derived neurotrophic factor (BDNF) in the habenula nucleus of depression-like rats induced by light deprivation. Methods: male SD rats were exposed to white light (white light control group, 20 rats) and constant darkness (depression model group, 60 rats), respectively. 18 days later rats in depression model group were randomly divided into three groups: depression model group (treated with constant darkness), blue light group (treated with blue light) and red light group (treated with red light). Rats in white light control group were kept in white light. All rats exposed to light were in a standard 12∶12 h Light/Dark condition at 20 lx for 36 days. Sucrose preference test was applied to evaluate depression-like symptoms of rats. The c-fos+cells in the habenula nucleus, intergeniculate leaflet and ventral lateral geniculate nucleus were detected. The phosphoylation of cAMP-response element binding protein (CREB) and the relative BDNF protein level in the habenula nucleus were measured. Results: Sucrose intake per kg body weight increased in rats exposed to blue light and returned to the level of control group (P>0.05). Sucrose intake per kg body weight in red light group and depression model group were lower than control group (P<0.05). More c-fos+cells were detected in the habenula nucleus, intergeniculate leaflet and ventral lateral geniculate nucleus from blue light group than those from depression model group (P<0.05). The relative BDNF protein level and the phosphoylation of CREB in the habenula nucleus from blue light group were higher than those from depression model group (P<0.05). Conclusion: Blue light could relieve depression-like symptoms in light-deprived rats. Exposure to blue light could activate neurons in the habenula nucleus to which intrinsically photosensitive retinal ganglion cells projected. Blue-light-mediated antidepressant effect might involve in the activation of CREB/BDNF signal transduction pathways in the habenula nucleus.
目的： 探讨蓝光照射对剥夺光照抑郁大鼠大脑缰核中脑源性神经营养因子（BDNF）的调节作用。 方法： 采用随机数字表法，将雄性SD大鼠随机分为白光对照组（20只）和抑郁模型组（60只），分别给予白光照射和剥夺光照处理；18 d后将抑郁模型组大鼠随机均分为抑郁模型组、蓝光处理组和红光处理组，分别给予剥夺光照、补充蓝光照射和补充红光照射处理。白光对照组继续给予白光照射。光照时长均为12 h/d，光照强度均为20 lx，处理持续36 d。期间采用蔗糖偏好试验检测动物的抑郁状态。分别测定各组大鼠大脑缰核、膝状体间叶和外侧膝状体腹侧核c-fos蛋白表达水平；测定缰核内环磷腺苷效应元件结合蛋白（CREB）磷酸化水平及下游蛋白BDNF表达水平。 结果： 补充光照后，蓝光处理组大鼠单位体重蔗糖摄入量基本恢复至白光对照组水平（P>0.05），红光处理组和抑郁模型组大鼠单位体重蔗糖摄入量均低于白光对照组（P值均<0.05）。蓝光处理组大鼠大脑缰核、膝状体间叶和外侧膝状体腹侧核c-fos阳性神经元密度均高于抑郁模型组（P值均<0.05）。蓝光处理组大鼠大脑缰核内BDNF相对表达量和CREB磷酸化水平均高于抑郁模型组（P值均<0.05）。 结论： 蓝光照射可缓解剥夺光照所致的大鼠抑郁样反应，蓝光可通过内在感光性视网膜神经节细胞激活缰核神经元反应，缰核中CREB/BDNF信号通路在蓝光抗抑郁效应中发挥重要作用。.