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 |
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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. |
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ISSN: | 0006-8993 1872-6240 |
DOI: | 10.1016/S0006-8993(97)01569-2 |