Fluoxetine inhibits dendrite atrophy of hippocampal neurons by decreasing nitric oxide synthase expression in rat depression model  

氟西汀通过降低一氧化氮合酶的表达而抑制抑郁症模型大鼠海马神经元树突萎缩(英文)

作　　者：罗兰[1] 谭仁祥[1] 

机构地区：[1]南京大学生命科学学院医药生物技术国家重点实验室,南京中国210093

出　　处：《Acta Pharmacologica Sinica》2001年第10期865-870,共6页中国药理学报（英文版）

基　　金：Project supported by the National Natural Science Foundation of China (No 39725033 and 39970083);Doctoral Training Program (No 1999028419);the Ministry of Education (No 1999-136)

摘　　要：AIM: To study the effect of fluoxetine on dendrite atrophy of hippocampal neurons in rat depression model. METHODS: CMS (chronic mild stress), mimicking human depression, was used as the animal depression model. The neurons shape and numbers of nitric oxide synthase positive cells in the hippocampal subfields were measured by Nissl staining and histochemical staining of NADPH (nicotinamide adenine dinucleotide phosphate)-diaphorase respectively. RESULTS: CMS deforms neurons in the hippocampal formation, and fluoxetine can renormalize the deformed neurons by inhibiting the nitric oxide synthase catalyzing the over-production of NO, which lead subsequently to the morphological abnormality in the circumscribed area of brain. CONCLUSION: Fluoxetine, an antidepressant, renormalizes dendrite atrophy of hippocampal neurons by inhibiting nitric oxide synthase overexpression in rat chronic mild stress model.目的:研究氟西汀对抑郁症大鼠模型的海马神经元树突萎缩的作用。方法:用慢性温和性应激模型作为抑郁症模型,采用尼氏染色观察海马各亚区神经无形态,用NADPH-d组化染色方法测定了海马中一氧化氮合酶阳性神经元的数量。结果:慢性温和性应激对海马神经元有一定的损伤,主要表现在神经元树突的萎缩,而氟西汀可使这些受损神经元恢复正常,这种作用与氟西汀抑制海马区的一氧化氮合酶阳性神经元的数量减少相关。结论:氟西汀可通过抑制海马区一氧化氮合酶的过度表达而阻止或扭转抑郁症模型大鼠海马神经元村突的萎缩。

关 键 词：FLUOXETINE antidepressive agents hippocampus neurons nitric-oxide synthase 

分 类 号：R96[医药卫生—药理学]