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首页> 外文期刊>The European Journal of Neuroscience >Estradiol suppresses rapid eye movement sleep and activation of sleep-active neurons in the ventrolateral preoptic area.
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Estradiol suppresses rapid eye movement sleep and activation of sleep-active neurons in the ventrolateral preoptic area.

机译：雌二醇抑制快速眼动睡眠和腹外侧前视区的睡眠活跃神经元的激活。

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Studies from multiple species, including humans, suggest that gonadal hormones, and ovarian hormones in particular, influence the physiology of sleep, but the mechanisms by which these hormones influence sleep behaviors are unknown. Previously, we demonstrated a 50% reduction in lipocalin-prostaglandin D synthase (L-PGDS) transcript levels, following estradiol treatment, at the level of the ventrolateral preoptic area (VLPO), a putative sleep-active nucleus. Catalytic activity of L-PGDS produces prostaglandin D(2) (PGD(2)), an endogenous somnogen. Based on our previous studies, we hypothesized that estradiol is acting via PGD(2) to suppress neuronal activity in the VLPO of females. To begin to test whether this is true, we quantified the number of Fos-immunopositive cells in hormonally manipulated male and female rats. We found that in females during the light phase, estradiol suppressed Fos expression in VLPO neurons. Interestingly, protein expression of L-PGDS followed the same pattern. Surprisingly,changes in the hormonal milieu of males had no effect. Using telemetry to record electroencephalograms from gonadally intact females, we found, in the light phase of proestrus when estradiol levels are high, a marked reduction in rapid eye movement (REM) sleep compared with the other days of the estrous cycle. However, during the dark phase of proestrus when estrogen and progesterone levels are elevated, significantly less time was spent in both non-REM and REM sleep. Thus, it seems that hormones in females play a major role in the regulation of sleep and arousal via activation of neurons in key sleep and arousal centers.
机译：来自包括人类在内的多个物种的研究表明，性腺激素，尤其是卵巢激素会影响睡眠的生理机能，但这些激素影响睡眠行为的机制尚不清楚。以前，我们证明在雌二醇处理后，脂蛋白-前列腺素D合酶（L-PGDS）转录水平在假定的睡眠活跃核腹侧前视区（VLPO）的水平降低了50％。 L-PGDS的催化活性产生前列腺素D（2）（PGD（2）），一种内源性的催眠剂。根据我们以前的研究，我们假设雌二醇通过PGD（2）来抑制女性VLPO中的神经元活性。为了测试这是否成立，我们量化了荷尔蒙操纵的雄性和雌性大鼠中Fos免疫阳性细胞的数量。我们发现在雌性动物的光照期，雌二醇抑制了VLPO神经元中Fos的表达。有趣的是，L-PGDS的蛋白质表达遵循相同的模式。令人惊讶的是，男性荷尔蒙环境的变化没有影响。我们使用遥测技术记录了性腺完好无损的女性的脑电图，发现在雌二醇水平较高时，处于发情前期的轻度阶段，与动情周期的其他几天相比，快速眼动（REM）睡眠明显减少。然而，在发情期的黑暗阶段，当雌激素和孕酮水平升高时，非快速眼动和快速眼动睡眠的时间明显减少。因此，似乎女性中的激素通过激活关键睡眠和唤醒中心的神经元，在睡眠和唤醒的调节中起主要作用。

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