Corticosterone attenuates zinc-induced neurotoxicity in primary hippocampal cultures

Primary hippocampal cultures derived from newborn rats were exposed to zinc chloride at 50, 75, 100, 150 and 200 μM concentrations. Neuronal injury was assessed morphologically and by the lactate dehydrogenase (LDH) efflux assay. Zinc exposure increased LDH efflux in a concentration-dependent manner...

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Veröffentlicht in:Brain research 1998-04, Vol.791 (1), p.295-298
Hauptverfasser: Sunanda, Rao, B.S.Shankaranarayana, Raju, T.R
Format: Artikel
Sprache:eng
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Zusammenfassung:Primary hippocampal cultures derived from newborn rats were exposed to zinc chloride at 50, 75, 100, 150 and 200 μM concentrations. Neuronal injury was assessed morphologically and by the lactate dehydrogenase (LDH) efflux assay. Zinc exposure increased LDH efflux in a concentration-dependent manner. Exposure to 100 μM zinc for 24 h resulted in beading of neurites and swelling of neuronal soma. When cultures were co-exposed to zinc at 100 μM and corticosterone in the range of 10 −5 to 10 −7 M, degeneration of neurons caused by zinc was attenuated. Our study suggests that corticosterone can protect neurons from zinc-induced neurotoxicity at low doses.
ISSN:0006-8993
1872-6240
DOI:10.1016/S0006-8993(97)01569-2