John J, Kumar V M
Department of Physiology, All India Institute of Medical Sciences, New Delhi, India.
Sleep. 1998 Sep 15;21(6):587-98. doi: 10.1093/sleep/21.6.587.
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.
本研究旨在确定N-甲基-D-天冬氨酸(NMDA)破坏内侧视前区(mPOA)神经元对大鼠睡眠-觉醒(S-W)、运动活动、体重、直肠温度以及食物和水摄入量的影响。mPOA的NMDA损伤导致长期失眠,包括异相睡眠在内的深度睡眠阶段显著减少。损伤大鼠睡眠发作持续时间的缩短表明它们无法维持睡眠。由睡眠压力降低引起的失眠并未改变睡眠启动能力。虽然睡眠的昼夜分布基本未受影响,但光照期的运动活动有所增加。mPOA损伤的大鼠不仅因多动而且因体温过高导致能量消耗增加,但其食物摄入量并未增加以进行补偿。因此,即使食物和水摄入量没有任何变化,大鼠的体重仍会减轻。然而,mPOA神经元丧失后体温和运动活动的变化可能并未对S-W产生重大影响,因为所有这些参数的变化具有不同的时间进程。