Mechanism of neurotoxicity by anesthetics in the developing brain-Effect of hypercapnia

为了研究新生儿暴露于低氧高碳酸血症对学习能力的可能长期后果，我们调查了新生儿低氧高碳酸血症对海马区后期功能的影响。新生大鼠(出生后7天；P7)暴露在高浓度二氧化碳(CO2；13%)中2或4小时。P7大鼠暴露在CO2中破坏了后来的学习获得，10周龄成年大鼠进行了Morris水迷宫测试。长时程增强(LTP)在海马CA1区突触的诱导也受到损害，而群体棘波的成对脉冲反应在CO2暴露的大鼠中显著增加。这种海马区突触可塑性的长期改变可能导致与围产期缺氧性高碳酸血症和酸中毒相关的学习障碍。

To investigate the possible long-term consequences of neonatal exposure to hypoxic hypercapnia regarding learning ability, we investigated the effect of neonatal hypoxic hypercapnia on later functions in the hippocampus. Neonatal rat pups (postnatal day 7; P7) were exposed to a high concentration of carbon dioxide (CO2; 13%) for 2 or 4 h. Exposure to CO2 in P7 rat pups disrupted later learning acquisition, as assessed in 10-week-old adult rats subjected to a Morris water maze test. Induction of long-term potentiation (LTP) in the synapses of the hippocampal CA1 area was also impaired, whereas the paired-pulse responses of population spikes exhibited a significant increase in CO2-exposed rats. Such long-lasting modifications in hippocampal synaptic plasticity may contribute to the learning impairments associated with perinatal hypoxic hypercapnia and acidosis.