Effects of vitamin E on lead-induced impairments in hippocampal synaptic plasticity

• Published in: Brain research 2015-12, Vol.1629, p.270-281
• Main Authors: Salehi, Iraj, Karamian, Ruhollah, Komaki, Alireza, Tahmasebi, Lida, Taheri, Masoumeh, Nazari, Masoumeh, Shahidi, Siamak, Sarihi, Abdolrahman
• Format: Article
• Language: English
• Subjects: Animals; Antioxidants; Antioxidants - pharmacology; Antioxidants - therapeutic use; Cognition Disorders - chemically induced; Cognition Disorders - drug therapy; Cognition Disorders - physiopathology; Dentate gyrus; Excitatory Postsynaptic Potentials - drug effects; Excitatory Postsynaptic Potentials - physiology; Hippocampus; Hippocampus - drug effects; Hippocampus - pathology; Hippocampus - physiology; Lead - toxicity; Lead acetate; Lipid Peroxidation - drug effects; Lipid Peroxidation - physiology; Long-term potentiation; Male; Neurology; Neuronal Plasticity - drug effects; Neuronal Plasticity - physiology; Rat; Rats; Rats, Wistar; Treatment Outcome; Vitamin E; Vitamin E - pharmacology; Vitamin E - therapeutic use
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/j.brainres.2015.10.007

Abstract Lead (Pb) exposure during development is associated with impaired cognitive function and long-term potentiation (LTP). Vitamin E (VE) is an antioxidant that could have protective effects against Pb intoxication. In this study, we examined the protective effects of vitamin E against Pb-induced LTP impairments. Forty-six adult male Wistar rats were randomly divided into 6 treatment groups: (1) control; (2) Pb exposure; (3) VE; (4) Pb +VE; (5) Pb exposure followed by VE 2 months after exposure; (6) VE followed by Pb exposure 1 month after treatment. Rats were exposed to Pb through daily consumption of Pb-contaminated distilled water; VE was administered by daily gavage for 3 months. After this period, the population spike (PS) amplitudes and the slopes of excitatory postsynaptic potentials (EPSPs) were measured in the dentate gyrus (DG) area of the hippocampus in adult rats in response to electrical stimulation applied to the perforant pathway in vivo. Blood samples were also collected to evaluate malondialdehyde (MDA) levels, total antioxidant capacity (TAC), and total oxidant status (TOS). Biochemical analyses demonstrated significant increases in plasma MDA and TOS levels in the Pb-exposed group compared to the control group. VE–protected groups revealed significant increases in TAC levels. Our results demonstrate that Pb decreased EPSP slopes and PS amplitudes compared to the control group, whereas VE increased these parameters compared to the control group. Co-administration of VE with Pb exposure inhibited Pb-induced effects. These findings suggest that VE via its antioxidant activity reverses Pb-induced impairments of synaptic plasticity in the DG.