光剥夺导致大鼠抑郁样改变及其机制研究

Effect of long-time light deprivation on depression and the possible pathological mechanism

目的探讨长时间光剥夺是否导致大鼠的抑郁样改变,并从中枢甘丙肽水平和神经元凋亡角度探讨可能的病理机制。方法随机选取实验组及对照组大鼠各12只,分别经持续避光及正常光照条件下饲养6周后,以强迫游泳实验中的静止时间判定大鼠的抑郁表现,以免疫荧光染色法检测大鼠脑部的甘丙肽水平及神经元凋亡情况。结果光剥夺组大鼠体重增加量及日均摄食量均低于光照组[(239.23±30.88)g vs(310.85±30.59)g,P<0.01;(31.25±2.10)g vs(39.55±1.51)g,P<0.01],在强迫游泳实验中的静止不动时间较光照组延长[(135.81±8.84)s vs(56.33±7.26)s,P<0.05],而中缝背核和蓝斑处的甘丙肽水平(以积分光密度表示)降低[(37.23±3.77)vs(29.25±2.95),P<0.05;(19.52±0.72)vs(5.13±2.68),P<0.01],但并未观察到神经元凋亡。结论长时间光剥夺可导致大鼠出现抑郁样表现,中枢甘丙肽水平的降低可能参与了这一过程。

Objective To investigate the impact of long-time light deprivation on depression-like behavior,and probe into the possible pathological mechanism with focus on central galanin level and apoptosis.Methods Twelve rats were kept in constant darkness for 6 weeks and 12 rats housed in a normal light-dark schedule served as controls.The immobility time in forced swim test（FST） was used to determine the extent of depression and immunofluorescence staining was employed to examine galanin expression as well as apoptotic neurons in the rat brain.Results Rats from the light deprivation group showed a decrease in both body-weight gain and food-intake compared with control rats [（239.23±30.88） g vs（310.85±30.59） g,P〈0.01;（31.25±2.10）g vs（39.55±1.51）g,P〈0.01].FST data showed that rats treated with 6 week-light deprivation showed a longer immobility time compared with controls [（135.81±8.84）s vs（56.33±7.26）s,P〈0.05].Immunofluorescence staining detected a reduction of galanin level,as evidenced by integral optical density,in the dorsal raphe nucleus and locus coeruleus [（37.23±3.77） vs（29.25±2.95）,P〈0.05;（19.52±0.72） vs（5.13±2.68）,P〈0.01],but not detect any apoptotic cell in the brain of rats treated with 6 week-light deprivation.Conclusions Long-time light deprivation leads to depression-like behavior in rats.The down-regulation of galanin level in the rat brain may be involved in long-time light deprivation-induced depression-like behavior.