In:
The Journal of Neuroscience, Society for Neuroscience, Vol. 24, No. 49 ( 2004-12-08), p. 11057-11069
Abstract:
Mechanisms that contribute to Na + influx during and immediately after 5 min anoxia were investigated in cultured rat hippocampal neurons loaded with the Na + -sensitive fluorophore sodium-binding benzofuran isophthalate. During anoxia, an influx of Na + in the face of reduced Na + ,K + -ATPase activity caused a rise in [Na + ] i . After the return to normoxia, Na + ,K + -ATPase activity mediated the recovery of [Na + ] i despite continued Na + entry. Sodium influx during and after anoxia occurred through multiple pathways and increased the longer neurons were maintained in culture. Under the experimental conditions used, Na + entry during anoxia did not reflect the activation of ionotropic glutamate receptors, TTX- or lidocaine-sensitive Na + channels, plasmalemmal Na + /Ca 2+ exchange, Na + /H + exchange, or \batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(\mathrm{HC}\mathrm{O}_{3}^{-}\) \end{document} -dependent mechanisms; rather, contributions were received from a Gd 3+ -sensitive pathway activated by reactive oxygen species and Na + /K + /2Cl - cotransport in neurons maintained for 6-10 and 11-14 d in vitro (DIV), respectively. Sodium entry immediately after anoxia was not attributable to the activation of ionotropic glutamate receptors, voltage-activated Na + channels, or Na + /K + /2Cl - cotransport; rather, it occurred via Na + /Ca 2+ exchange, Na + /H + exchange, and a Gd 3+ -sensitive pathway similar to that observed during anoxia; 11-14 DIV neurons received an additional contribution from an \batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(\mathrm{HC}\mathrm{O}_{3}^{-}\) \end{document} -dependent mechanism(s). The results provide insight into the intrinsic mechanisms that contribute to disturbed internal Na + homeostasis during and immediately after anoxia in rat hippocampal neurons and, in this way, may play a role in the pathogenesis of anoxic or ischemic cell injury.
Type of Medium:
Online Resource
ISSN:
0270-6474
,
1529-2401
DOI:
10.1523/JNEUROSCI.2829-04.2004
Language:
English
Publisher:
Society for Neuroscience
Publication Date:
2004
detail.hit.zdb_id:
1475274-8
SSG:
12
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