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- W2006558812 abstract "Neonatal rats survive and avoid brain injury during periods of anoxia 25 times longer than adults. We hypothesized that oxygen activates and hypoxia suppresses NMDA receptor (NMDAR) responses in neonatal rat neurons, explaining the innate hypoxia tolerance of these cells. In CA1 neurons isolated from neonatal rat hippocampus (mean postnatal age [P] 5.8 days), hypoxia (PO2 10 mm Hg) reduced NMDA receptor-channel open-time percentage and NMDA-induced increase in [Ca2+]i (NMDA ΔCa2+) by 38 and 68% (P<0.01), respectively. In P20 neurons the reductions were not significant. In P3–10 CA1 neurons within intact hippocampal slices, hypoxia reduced NMDA ΔCa2+ by 52% (P=0.002) and decreased NMDA-induced death by 45% (P=0.004). Phalloidin, a microtubule stabilizer, prevented hypoxia-induced inhibition of NMDA ΔCa2+ in P3–10 neurons. To test whether NMDARs prevalent in neonates (NR1 plus NR2B or NR2D subunits) are inhibited by hypoxia compared with those in mature neurons (NR2A and NR2C), we expressed these receptors in Xenopus oocytes. Compared with responses in 21% O2, hypoxia (PO2 17 mm Hg) reduced currents from neonatal type NR1/NR2D receptors by 25%, increased currents from NR1/NR2C by 18%, and had no effect on NR1/NR2A or NR1/NR2B. Modulation of NMDARs by hypoxia may play an important role in the hypoxia tolerance of the mammalian neonate. In addition, oxygen sensing by NMDARs could play a significant role in postnatal brain development." @default.
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- W2006558812 date "1995-04-01" @default.
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- W2006558812 title "Reverse transcriptase activity in human lymphocytes and brain tissue" @default.
- W2006558812 doi "https://doi.org/10.1016/0920-9964(95)95173-7" @default.
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