Rao B S, Raju T R
Department of Neurophysiology, National Institute of Mental Health and Neuro Sciences, Bangalore 560 029, India.
Brain Res. 1998 Apr 27;791(1-2):295-8. doi: 10.1016/s0006-8993(97)01569-2.
Primary hippocampal cultures derived from newborn rats were exposed to zinc chloride at 50, 75, 100, 150 and 200 microM 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 microM zinc for 24 h resulted in beading of neurites and swelling of neuronal soma. When cultures were co-exposed to zinc at 100 microM 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.
将新生大鼠的原代海马体培养物暴露于浓度为50、75、100、150和200微摩尔的氯化锌中。通过形态学和乳酸脱氢酶（LDH）外排试验评估神经元损伤。锌暴露以浓度依赖的方式增加LDH外排。暴露于100微摩尔锌24小时导致神经突串珠样改变和神经元胞体肿胀。当培养物同时暴露于100微摩尔锌和浓度范围为10⁻⁵至10⁻⁷摩尔的皮质酮时，锌引起的神经元变性减弱。我们的研究表明，低剂量的皮质酮可以保护神经元免受锌诱导的神经毒性。
