突触发生
抗抑郁药
神经科学
海马体
NMDA受体
前额叶皮质
谷氨酸受体
心情
敌手
心理学
氯胺酮
萧条(经济学)
医学
认知
精神科
受体
内科学
宏观经济学
经济
作者
Ronald S. Duman,George K. Aghajanian
出处
期刊:Science
[American Association for the Advancement of Science (AAAS)]
日期:2012-10-05
卷期号:338 (6103): 68-72
被引量:1222
标识
DOI:10.1126/science.1222939
摘要
Basic and clinical studies demonstrate that depression is associated with reduced size of brain regions that regulate mood and cognition, including the prefrontal cortex and the hippocampus, and decreased neuronal synapses in these areas. Antidepressants can block or reverse these neuronal deficits, although typical antidepressants have limited efficacy and delayed response times of weeks to months. A notable recent discovery shows that ketamine, a N-methyl-D-aspartate receptor antagonist, produces rapid (within hours) antidepressant responses in patients who are resistant to typical antidepressants. Basic studies show that ketamine rapidly induces synaptogenesis and reverses the synaptic deficits caused by chronic stress. These findings highlight the central importance of homeostatic control of mood circuit connections and form the basis of a synaptogenic hypothesis of depression and treatment response.
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