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Effect of NMDA lesion of the medial preoptic neurons on sleep and other functions.

机译:内侧视前神经元的NMDA损伤对睡眠和其他功能的影响。

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摘要

This study was undertaken to determine the effects of the destruction of the medial preoptic area (mPOA) neurons by N-methyl D-aspartic acid (NMDA), on sleep-wakefulness (S-W), locomotor activity, body weight, rectal temperature, and food and water intake in rats. The NMDA lesion of the mPOA produced long-lasting insomnia with marked reduction in the deeper stages of sleep, including paradoxical sleep. The reduction in the duration of sleep episodes in the lesioned rats indicated their inability to maintain sleep. The insomnia resulting from a decreased sleep pressure did not alter the sleep-initiating ability. Though the day-night distribution of sleep remained largely unaffected, there was an increase in locomotor activity during the light period. There was no increase in food intake to compensate for the high energy expenditure resulting not only from hyperactivity but also from hyperthermia in the mPOA-lesioned rats. Thus, body weights of the rats were reduced even without any change in food and water intake. However, the changes in body temperature and locomotor activity after the mPOA neuronal loss may not have exerted a major influence on S-W, as the alterations in all these parameters had different time courses.
机译:进行这项研究来确定N-甲基D-天冬氨酸(NMDA)破坏内侧视前区(mPOA)神经元对睡眠-清醒(SW),运动能力,体重,直肠温度和大鼠食物和水的摄入量。 mPOA的NMDA病变产生了长期的失眠,并在包括反常性睡眠在内的深层睡眠中明显减少。患病大鼠睡眠发作持续时间的减少表明它们无法维持睡眠。睡眠压力降低导致的失眠并没有改变睡眠启动能力。尽管昼夜睡眠分布在很大程度上未受影响,但在轻度时期自发活动有所增加。食物摄入量没有增加,以补偿高能量消耗,不仅是由于过度活跃,而且是mPOA损伤大鼠的体温过高引起的。因此,即使食物和水摄入量没有任何变化,大鼠的体重也减少了。但是,mPOA神经元丧失后体温和运动能力的变化可能未对S-W产生重大影响,因为所有这些参数的变化都具有不同的时程。

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