Monosialoanglioside (GM1) prevents lead-induced neurotoxicity on long-term potentiation, SOD activity, MDA levels, and intracellular calcium levels of hippocampus in rats

摘要

Lead (Pb2+) is one of the most common neurotoxic metals present in our environment. Chronic or acute exposure to Pb2+ causes impairment to the central nervous system (CNS). As one potent useful tool in the attempt to protect against impairment and promote functional recovery of the CNS, gangliosides are hopeful for recovering Pb2+ neurotoxicity. The aim of this study is to investigate the effects of monosialoganglioside (GM1) on the Pb2+-induced impairments of synaptic plasticity, antioxidant system function, and intracellular calcium levels in the hippocampus of acute Pb2+-exposed rats. Our study showed that: (1) Acute Pb2+ exposure impaired synaptic transmission and plasticity in the hippocampus and GM1 preconditioning rescued to some extent this impairment in urethane-anesthetized rats. (2) Superoxide dismutase activities and malondialdehyde levels were significantly increased in the acute Pb2+-exposed hippocampus which could be reduced by GM1 preconditioning. (3) Further, acute Pb2+ exposure caused the internal free Ca2+ fluctuation in the cultured hippocampal neurons and GM1 preconditioning could abate this fluctuation. Taken together, our results illustrated the possible mechanisms underlying the protective effects of GM1 against Pb2+ neurotoxicity and might shed light on protection against Pb2+ toxicity and its treatment. Keywords Ganglioside GM1 - Pb2+ - Long-term potentiation - Internal calcium levels - Antioxidant system