Sechenov Institute of Evolutionary Physiology and Biochemistry of RAS (IEPhB), 44, Toreza pr., Saint Petersburg 194223, Russia.
Sechenov Institute of Evolutionary Physiology and Biochemistry of RAS (IEPhB), 44, Toreza pr., Saint Petersburg 194223, Russia; Institute of Experimental Medicine, Almazov National Medical Research Centre, 2 Akkuratova Street, Saint Petersburg 197341, Russia.
Neurobiol Learn Mem. 2019 Oct;164:107066. doi: 10.1016/j.nlm.2019.107066. Epub 2019 Aug 7.
Prenatal hypoxia often results in dramatic alterations in developmental profiles and behavioral characteristics, including learning and memory, in later life. Despite the accumulation of considerable amounts of experimental data, the mechanisms underlying developmental deficits caused by prenatal hypoxia remain unclear. In the present study, we investigated whether prenatal hypoxia on embryonic day 14 (E14) affected synaptic properties in the hippocampus and hippocampal-related cognitive functions in young rats. We found that 20- to 30-d-old rats subjected to prenatal hypoxia had significantly disturbed basal synaptic transmission in CA3-CA1 synapses and a two-fold decrease in hippocampal long-term synaptic potentiation. These alterations were accompanied by a significant decline in the protein level of GluN2B but not GluN2A NMDA receptor subunits. In addition, the number of synaptopodin-positive dendritic spines in the CA1 area of the hippocampus was reduced in the rats exposed to prenatal hypoxia. These changes resulted in significant learning and memory deficits in a novel object recognition test.
产前缺氧通常会导致发育模式和行为特征的显著改变，包括学习和记忆，在以后的生活中。尽管积累了大量的实验数据，但产前缺氧引起的发育缺陷的机制仍不清楚。在本研究中，我们研究了胚胎第 14 天 (E14) 的产前缺氧是否会影响年轻大鼠海马中的突触特性和与海马相关的认知功能。我们发现，20 至 30 日龄的产前缺氧大鼠 CA3-CA1 突触的基础突触传递明显受到干扰，海马长时程突触增强作用降低了两倍。这些变化伴随着 GluN2B 而不是 GluN2A NMDA 受体亚单位的蛋白水平显著下降。此外，暴露于产前缺氧的大鼠海马 CA1 区的突触小体阳性树突棘数量减少。这些变化导致在新物体识别测试中出现明显的学习和记忆缺陷。
