GABA能系统在应激诱发的抑郁症中的作用
The role of stress-induced GABAergic system alteration in depression
查看参考文献64篇
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文摘
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¡-氨基丁酸(γ-aminobutyric acid, GABA)是中枢神经系统中最重要的抑制性神经递质,在维持大脑的兴奋–抑制平衡中起到重要作用。越来越多的临床和基础研究显示抑郁症与各种GABA能神经元活动不足相关,抗抑郁药物可以缓解或恢复上述变化。GABA能系统延迟发育至成年早期基本成熟。应激,尤其是早期应激是抑郁症发病的重要风险因素,可以通过扰动GABA能系统的发育轨迹从而造成对该系统结构和功能的持续后果,并与后期抑郁症易感密切相关。未来的研究需要进一步鉴别二者之间的关系,进而提出以GABA能系统为靶标的抑郁症治疗新策略。 |
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其他语种文摘
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γ-aminobutyric acid (GABA) is the most important inhibitory amino acid neurotransmitter in the central nervous system to maintain the excitatory-inhibitory balance of the brain. Increasing clinical and pre-clinical evidence shows a central and causal role of GABAergic deficits in depressive disorders. Depressive patients commonly indicate reduced GABAergic transmission in emotional and cognitive brain areas, especially prefrontal cortex and limbic areas like hippocampus and amygdala, and antidepressants can alleviate or reverse depressive symptoms by augmenting GABAergic activity in these areas. Furthermore, deficits in GABAergic transmission are sufficient to cause most of the neural and behavioral alterations expected in an animal model of depression. GABAergic system undergoes a prolonged development to structural and functional maturation until into early adulthood in both human and rodents. Stress, especially early stress, may disturb the mature trajectory of the GABAergic system, and result in continuing negative consequences of neural development and late functioning, which can contribute to the increased susceptibility for the onset of depression across late life. It would be important to further elucidate GABAergic mechanisms underlying depressive disorders and action of antidepressant in order to improve strategy for early recognition and intervention of depression. |
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来源
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心理科学进展
,2017,25(12):2075-2081 【核心库】
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DOI
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10.3724/SP.J.1042.2017.02075
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关键词
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应激
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GABA能系统
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抑郁症
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地址
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1.
中国科学院心理研究所, 中国科学院心理健康重点实验室, 北京, 100101
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西南大学心理学部, 认知与人格教育部重点实验室, 重庆, 400715
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语种
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中文 |
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文献类型
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研究性论文 |
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ISSN
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1671-3710 |
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学科
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社会科学总论 |
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基金
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国家自然科学基金
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中国科学院项目
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中国科学院心理健康重点实验室(中国科学院心理研究所)资助
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文献收藏号
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CSCD:6130752
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