色氨酸对应激小鼠空间学习能力和下丘脑单胺类递质的影响

目的:研究色氨酸对慢性应激抑郁模型小鼠空间学习记忆、下丘脑单胺类神经递质(5-HT,NE)及糖水偏爱度的影响。方法:应用慢性不可预见性刺激结合孤养4周的方法建立慢性应激抑郁小鼠模型,小鼠随机分为空白对照组(NC)、应激抑郁模型组(CUS)、应激抑郁模型+低剂量色氨酸(CUS-L)组、应激抑郁模型+高剂量色氨酸(CUS-H)组。水迷宫实验测定小鼠空间学习记忆的能力,称取胸腺和脾脏测定胸腺和脾脏指数,ELISA法检测下丘脑5-羟色胺(5-HT)、去甲肾上腺素(NE)的含量。结果:与对照组相比,模型组小鼠下丘脑中5-HT水平降低,NE含量升高;对糖水的偏爱度下降;胸腺、脾脏指数降低;与模型组相比,实验组5-HT水平升高,NE含量降低;对糖水的偏爱度增加;胸腺、脾脏指数升高。结论:色氨酸可提高应激抑郁模型小鼠空间学习记忆能力,增加其对糖水的偏爱性,同时使下丘脑中5-HT含量增加,NE含量减少,脏器指数的变化提示色氨酸有抗应激作用,并对机体免疫起调节作用。

Effect of tryptophan on spatial learning ability and hypothalamus monoamine neural transmitter of depression model mice

Objective:Experiments were conducted to investigate the effect of tryptophan on spatial learning and memory ability,monoamine neural transmitter level(5-HT,NE)in hypothalamus and sugar water preferences of depression model mice.Methods:Stress depression model was established by the application of Chronic Unpredictable Stress(CUS)and solitary raised for 4 weeks.60 mice were divided randomly into 4 groups:the normal control(NC)group,chronic unpredictable stress(CUS)group,chronic unpredictable stress with low-dose tryptophan(CUS-L)group,chronic unpredictable stress with high-dose tryptophan(CUS-H)group.Morris water maze was used to assess spatial learning and memory ability,then weighed organs and calculate organs/body weight ratio,content of 5-HT and NE in hypothalamus were detected by ELISA method.Results:Compared with NC group,5-HT level,sugar water preferences and organs/body weight ratio significantly reduced while NE level was increased in CUS group;in both CUS-L and CUS-H groups,after irrigation stomach tryptophan for 28d,not only 5-HT level,sugar water preferences but also organs/body weight ratio were significantly increased,however,NE concentration was declined.Conclusion:For depressed model mice,tryptophan could enhance mice spatial learning and memory ability,increase its preference for sugar water,improve 5-HT level but reduce NE level in hypothalamus,and changes of visceral index meant that tryptophan had the role of anti-stress as well as immune regulation.