Lack of effects of vitamin E on aluminium-induced deficit of synaptic plasticity in rat dentate gyrus in vivo

Abstract

Aluminium (Al), has the potential to be neurotoxic in humans and animals, and is present in many manufactured foods and medicines and is also added to drinking water for purification purposes. Our previous study demonstrated that chronic Al exposure induced deficits of both long-term potentiation (LTP) and long-term depression (LTD) of excitatory postsynaptic potential (EPSP) and population spike (PS) in rat dentate gyrus (DG) of hippocampus in vivo (Wang et al., 2001). The purpose of the present study was to investigate whether the Al-induced impairment of synaptic plasticity could be reversed by dietary supplementation with vitamin E (Vit E; α-tocopherol). Neonatal Wistar rats were exposed to Al from parturition throughout life by drinking 0.3% aluminium chloride (AlCl 3) solution or a diet supplemented with Vit E at 500 μg/g/day with 0.3% AlCl 3. The input/output (I/O) function, EPSP and PS were measured in DG area of adult rats (80–100 days of age) in response to stimulation applied to the lateral perforant path. The results showed that: (1) chronic Al exposure reduced the amplitudes of both EPSP LTP (control: 130.4±3%, n=7; Al-exposed: 110±2%, n=9, P<0.001) and PS LTP (control: 241±19%, n=7; Al-exposed: 130±7%, n=9, P<0.001) significantly. Vit E had no significant effects on the Al-induced deficits of EPSP LTP (Al-exposed: 110±2%, n=9; Al-exposed+Vit E: 112±2%, n=8, P>0.05) and PS LTP (Al-exposed: 130±7%, n=9; Al-exposed+Vit E: 129±4%, n=8; P>0.05); (2) the amplitudes of EPSP LTD (control: 84±4%, n=7; Al-exposed: 92±7%, n=9, P<0.01) and PS LTD (control: 81±4%, n=7; Al-exposed: 98±5%, n=9, P<0.001) were also decreased by Al treatment. The impaired EPSP LTD (Al-exposed: 92±7%, n=9; Al-exposed+Vit E: 93±4%, n=8, P>0.05) and PS LTD (Al-exposed: 98±5%, n=9; Al-exposed+Vit E: 94±6%, n=8, P>0.05) were also not significantly affected by Vit E treatment. It was suggested that dietary supplementation with Vit E did not reverse the impairment of synaptic plasticity induced by Al in DG in vivo.