Depoortere H, Françon D, Llopis J
Synthelabo Recherche (LERS), Bagneux, France.
Neuropsychobiology. 1993;27(4):237-45. doi: 10.1159/000118988.
The influence of magnesium, one of the most important cations in the vertebrate body, on the sleep-wakefulness cycle and ECoG patterns in chronically implanted rats recorded during the light period over a 6-hour period was investigated. Two groups of rats were studied. Group 1 (6 rats): after a control period of 2 weeks, the rats were maintained for 9 weeks on a Mg(2+)-deficient diet. Group 2 (5 rats): after a control period of 2 weeks, the rats were maintained for 7 weeks on a Mg(2+)-deficient diet followed by 4 weeks on a normal diet (recovery period: weeks 8-11). Mg(2+)-deficient diet for 9 weeks induced sleep and ECoG time-dependent alterations. After 6-7 weeks on a Mg(2+)-deficient diet (n = 11) sleep analysis showed a significant increase of wakefulness (+50%) at the expense of slow wave sleep (-24%) but paradoxical sleep was not significantly modified. After 9 weeks of a Mg2+ deficient diet, sleep was disorganized: light sleep and polyspikes occurred indicating an increase in neuronal excitability. When Mg2+ was reintroduced in food and water, sleep organization and ECoG recordings were restored to their original patterns. Our findings which are in line with previous clinical and pharmacological observations provide conclusive arguments for the neuroprotective effect of magnesium ions in neurologic disorders and epileptiform activity. Mg2+ deficiency induces ECoG alterations in the rat which bear some similarities with those seen in neurogenic spasmophilic syndromes in man.
镁是脊椎动物体内最重要的阳离子之一,本研究调查了其对在光照期慢性植入大鼠6小时期间睡眠-觉醒周期及脑电图(ECoG)模式的影响。研究了两组大鼠。第1组(6只大鼠):在2周的对照期后,大鼠在缺镁(Mg2+)饮食条件下维持9周。第2组(5只大鼠):在2周的对照期后,大鼠在缺镁饮食条件下维持7周,随后在正常饮食条件下维持4周(恢复期:第8 - 11周)。9周的缺镁饮食诱导了睡眠和ECoG的时间依赖性改变。在缺镁饮食6 - 7周后(n = 11),睡眠分析显示清醒时间显著增加(+50%),代价是慢波睡眠减少(-24%),但异相睡眠无显著改变。在缺镁饮食9周后,睡眠变得紊乱:出现浅睡眠和多棘波,表明神经元兴奋性增加。当食物和水中重新添加Mg2+后,睡眠结构和ECoG记录恢复到原始模式。我们的发现与先前的临床和药理学观察结果一致,为镁离子在神经系统疾病和癫痫样活动中的神经保护作用提供了确凿证据。Mg2+缺乏在大鼠中诱导ECoG改变,这些改变与人神经源性痉挛性综合征中所见的改变有一些相似之处。