Deactivation by benzodiazepine of the basal forebrain and amygdala in normal humans during sleep:: A placebo-controlled [15O]H2O PET study
Deactivation by benzodiazepine of the basal forebrain and amygdala in normal humans during sleep:: A placebo-controlled [15O]H2O PET study
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DOI：
10.1176/appi.ajp.161.4.748
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发表时间：
2004-04-01
影响因子：
17.7
通讯作者：
Takahashi, K
中科院分区：
文献类型：
--
作者：
Kajimura, N;Nishikawa, M;Takahashi, K
目的：作者的目的是确定生理睡眠和苯二氮卓类药物诱导睡眠之间大脑区域活动的差异，以阐明与药物催眠作用有关的大脑结构。方法：在双盲交叉设计中，他们使用正电子发射断层扫描，比较了9名志愿者在非快速眼动睡眠期间的脑区域血流量，这些志愿者分别服用安慰剂或短效苯二氮卓类药物三唑仑。结果：在非快速眼动睡眠期间，服用三唑安定的受试者基底前脑和杏仁核复合物的血流量低于服用安慰剂的受试者。结论：苯二氮卓类药物的催眠作用可能主要与前脑清醒控制系统失活有关，也可能与情绪中枢失活引起的焦虑作用有关。
Objective: The authors' goal was to identify differences in regional brain activity between physiological and benzodiazepine-induced sleep to clarify the brain structures involved in the drug's hypnotic effect.Method: Using positron emission tomography, they compared regional cerebral blood flow during non-REM sleep in nine volunteers treated with placebo or triazolam, a short-acting benzodiazepine, in a double-blind, crossover design.Results: Blood flow in the basal forebrain and amygdaloid complexes was lower during non-REM sleep when subjects were given triazolam than when they were given placebo.Conclusions: The hypnotic effect of the benzodiazepines may be mediated mainly by deactivation of the forebrain control system for wakefulness and also by the anxiolytic effect induced by deactivation of the emotional center.