Kajimura Naofumi, Nishikawa Masami, Uchiyama Makoto, Kato Masaaki, Watanabe Tsuyoshi, Nakajima Toru, Hori Toru, Nakabayashi Tetsuo, Sekimoto Masanori, Ogawa Kenichi, Takano Harumasa, Imabayashi Etsuko, Hiroki Masahiko, Onishi Takashi, Uema Takeshi, Takayama Yutaka, Matsuda Hiroshi, Okawa Masako, Takahashi Kiyohisa
National Center Hospital for Mental, Neervous and Muscular Disorders, Kodaira, Tokyo, Japan.
Am J Psychiatry. 2004 Apr;161(4):748-51. doi: 10.1176/appi.ajp.161.4.748.
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.
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.
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.
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.
作者的目标是确定生理睡眠和苯二氮䓬诱导睡眠之间区域脑活动的差异,以阐明参与该药物催眠作用的脑结构。
他们采用正电子发射断层扫描技术,在双盲、交叉设计中,比较了9名接受安慰剂或短效苯二氮䓬三唑仑治疗的志愿者在非快速眼动睡眠期间的局部脑血流量。
与给予安慰剂相比,给予三唑仑的受试者在非快速眼动睡眠期间,基底前脑和杏仁核复合体的血流量较低。
苯二氮䓬类药物的催眠作用可能主要通过使觉醒的前脑控制系统失活,以及通过使情感中枢失活所诱导的抗焦虑作用来介导。