Department of Neurology, University of Vermont, Burlington, VT 05405, USA.
Exp Neurol. 2012 Apr;234(2):398-404. doi: 10.1016/j.expneurol.2012.01.005. Epub 2012 Jan 16.
Preeclampsia is a hypertensive disorder of pregnancy that affects many organs including the brain. Neurological complications occur during preeclampsia, the most serious of which is seizure known as eclampsia. Although preeclampsia can precede the eclamptic seizure, it often occurs during normal pregnancy, suggesting that processes associated with normal pregnancy can promote neuronal excitability. Here we investigated whether circulating inflammatory mediators that are elevated late in gestation when seizure also occurs are hyperexcitable to neuronal tissue. Evoked field potentials were measured in hippocampal slices in which control horse serum that slices are normally grown in, was replaced with serum from nonpregnant or late-pregnant Wistar rats for 48 h. We found that serum from pregnant, but not nonpregnant rats, caused hyperexcitability to hippocampal neurons and seizure activity that was abrogated by inhibition of tumor necrosis factor alpha (TNFα) signaling. Additionally, application of TNFα mimicked this increased excitability. Pregnant serum also caused morphological changes in microglia characteristic of activation, and increased TNFα mRNA expression that was not seen with exposure to nonpregnant serum. However, TNFα protein was not found to be elevated in pregnant serum itself, suggesting that other circulating factors during pregnancy caused activation of hippocampal slice cells to produce a TNFα-mediated increase in neuronal excitability. Lastly, although pregnant serum caused neuroinflammation and hyperexcitability of hippocampal slices, it did not increase blood-brain barrier permeability, nor were pregnant rats from which the serum was taken undergoing seizure. Thus, the BBB has an important role in protecting the brain from circulating neuroinflammatory mediators that are hyperexcitable to the brain during pregnancy. These studies provide novel insight into the underlying cause of eclampsia without elevated blood pressure and the protective role of the BBB that prevents exposure of the brain to hyperexcitable factors.
子痫前期是一种妊娠高血压疾病,会影响包括大脑在内的许多器官。子痫前期会出现神经系统并发症,其中最严重的是癫痫发作,称为子痫。虽然子痫前期可能先于癫痫发作,但它通常发生在正常妊娠期间,这表明与正常妊娠相关的过程可能会促进神经元兴奋性。在这里,我们研究了在癫痫发作时升高的循环炎症介质是否对神经元组织过度兴奋。在海马切片中测量了诱发场电位,其中用来自非妊娠或妊娠晚期 Wistar 大鼠的血清替代了正常切片生长的马血清 48 小时。我们发现,来自妊娠大鼠的血清而非非妊娠大鼠的血清导致海马神经元过度兴奋和癫痫发作,而肿瘤坏死因子α(TNFα)信号通路的抑制可消除这种作用。此外,应用 TNFα模拟了这种兴奋性增加。妊娠血清还导致小胶质细胞发生形态变化,表现出激活特征,并增加 TNFα mRNA 表达,但与暴露于非妊娠血清时不同。然而,未在妊娠血清本身中发现 TNFα 蛋白升高,这表明在妊娠期间其他循环因子导致海马切片细胞激活,产生 TNFα 介导的神经元兴奋性增加。最后,尽管妊娠血清导致海马切片的神经炎症和过度兴奋,但它并未增加血脑屏障通透性,也未导致从中提取血清的妊娠大鼠发生癫痫发作。因此,BBB 在保护大脑免受循环神经炎症介质的过度兴奋方面起着重要作用,而这些介质在妊娠期间对大脑具有兴奋性。这些研究为没有血压升高的子痫和 BBB 防止大脑暴露于过度兴奋因子的保护作用的根本原因提供了新的见解。