Hypoxia-tolerant neonatal CA1 neurons: relationship of survival to evoked glutamate release and glutamate receptor-mediated calcium changes in hippocampal slices

Brain Research. Developmental Brain Research
P E Bickler, B M Hansen

Abstract

Neurons in the neonatal mammalian brain survive greater degrees of hypoxic stress than those in the mature brain. To investigate how developmental changes in glutamate receptor-mediated neurotoxicity contribute to this difference, we measured hypoxia-evoked glutamate release, glutamate receptor contribution to hypoxia-evoked intracellular calcium changes, and survival of hypoxia-/ischemia-sensitive CA1 neurons in rat hippocampus. Glutamate release was measured by a fluorescence assay, calcium changes in CA1 neurons with fura-2, and cell viability using Nissl and fluorescence staining with calcein-AM/ethidium homodimer, all in 300-micron thick hippocampal slices from 3-30 post-natal day (PND) rats. Glutamate released from PND 3-7 slices during hypoxia (PO2 = 5 mmHg) was only one third that of PND 18-22 slices. In PND 3-7 slices, survival of CA1 neurons after 5 min of hypoxia and 6 h of recovery was significantly greater than in PND 18-22 slices (viability indices 0.60 and 0.28, respectively, (p < 0.05). Five min of anoxia significantly altered Nissl staining pattern and morphology of CA1 neurons in PND 18-22 but not PND 3-7 slices. Hypoxia (PO2 = 5 mm Hg) caused three to five times greater increases in [Ca2+]i in PND 18-22 slice...Continue Reading

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Citations

May 12, 2012·Journal of Comparative Physiology. B, Biochemical, Systemic, and Environmental Physiology·Mark BandAaron Avivi
May 7, 2004·Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism·Göran E Nilsson, Peter L Lutz
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