Repairing And Protective Effects Of Ganglioside On Lead Induced Impairment On Synaptic Plasticity Of Hippocampus In Rats

Lead is one of the most common neurotoxic metals present in our environment, which causes impairment to the central nervous system(CNS).Of great importance is how to diminish the impairment on CNS induced by lead.Gangliosides are particularly abundant in nervous system and play a variety of important roles in regulating proliferation,neurogenesis and synaptic transmission.The purpose of this study is to evaluate the repairing and protective effect of ganglioside on the lead-induced impairment of synaptic plasticity.The results show that:1.The effects of ganglioside on the lead-induced impairments of LTP and DP were evaluated in rat dentate gyrus in vivo.The experiments were carried out in three groups of rats(control,chronic lead-exposed,ganglioside treated lead-exposed, respectively).The input-output(I/O) function,pair-pulses reaction,excitatory postsynaptic potential(EPSP) and population spike(PS) amplitude were measured in the dentate gyrus(DG) of adult rats in response to stimulation applied to the lateral perforant path.The results showed that:(1).chronic lead exposure impaired LTP/DP measured on both EPSP slope and PS amplitude in DG area of the hippocampus.(2). the amplitudes of LTP/DP of lead-exposed group were significantly increased by supplying ganglioside.These results suggested intraperitoneally injection with ganglioside could repair the lead-induced impairments of synaptic plasticity in rats partyly and ganglioside might be one effective agent in repairing the lead induced impairment on synaptic plasticty.2.The effects of monosialoganglioside(GM1) were studied on synaptic plasticity, antioxidant system function and intracellular calcium levels in the hippocampus of acute Pb²⁺ exposed rats by electrophysiological recordings in vivo,biochemical analysis and confocal image analysis in vitro.The experiments were carried out in five groups of rats(Blank control,Saline control,Acute lead exposed,GM1 control and GM1 treaed acute lead exposed).The results showed that:(1) Acute lead exposure impaired synaptic transmission(I/O and baseline) and plasticity(LTP) in the hippocampus and GM1 preconditioning rescued to some extent this impairment in urethane anesthetized rats.(2) Superoxide dismutase(SOD) activities and malondialdehyde(MDA) levels were significantly increased in the acute-Pb²⁺-exposed hippocampus which could be reduced by GM1 preconditioning. (3) Acute Pb²⁺ exposure caused the internal free Ca²⁺ fluctuation in the cultured hippocampal neurons and GM1 preconditioning could abate this fluctuation.Taken together,GM1 preconditioning could reduce the acute lead induced impairment on synapstic plasiticity and cell function,GM1 might be one useful tool in protecting against Pb²⁺ toxicity and its treatment.