维生素E对大鼠体内铝诱导的齿状回突触可塑性缺陷无影响。

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

作者信息

Wang Ming, Ruan Di-Yun, Chen Ju-Tao, Xu Yao-Zhong

机构信息

School of Life Science, University of Science and Technology of China, Hefei, 230027, Anhui, PR China.

出版信息

Food Chem Toxicol. 2002 Apr;40(4):471-8. doi: 10.1016/s0278-6915(01)00094-1.

DOI:10.1016/s0278-6915(01)00094-1

PMID:11893406

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; alpha-tocopherol). Neonatal Wistar rats were exposed to Al from parturition throughout life by drinking 0.3% aluminium chloride (AlCl3) solution or a diet supplemented with Vit E at 500 microg/g/day with 0.3% AlCl3. 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.

摘要

铝（Al）对人类和动物具有神经毒性，存在于许多加工食品和药品中，并且为了净化目的也被添加到饮用水中。我们之前的研究表明，长期铝暴露会导致大鼠海马齿状回（DG）体内兴奋性突触后电位（EPSP）和群体峰电位（PS）的长时程增强（LTP）和长时程抑制（LTD）均出现缺陷（Wang等人，2001年）。本研究的目的是调查通过饮食补充维生素E（Vit E；α-生育酚）是否可以逆转铝诱导的突触可塑性损伤。新生Wistar大鼠从分娩开始终生饮用0.3%氯化铝（AlCl3）溶液或饮用添加了500μg/g/天Vit E和0.3% AlCl3的饮食，从而暴露于铝环境中。在成年大鼠（80 - 100日龄）的DG区域测量输入/输出（I/O）功能、EPSP和PS，以响应施加到外侧穿通路径的刺激。结果表明：（1）长期铝暴露显著降低了EPSP LTP（对照组：130.4±3%，n = 7；铝暴露组：110±2%，n = 9，P < 0.001）和PS LTP（对照组：241±19%，n = 7；铝暴露组：130±7%，n = 9，P < 0.001）的幅度。Vit E对铝诱导的EPSP LTP缺陷（铝暴露组：110±2%，n = 9；铝暴露 + Vit E组：112±2%，n = 8，P > 0.05）和PS LTP缺陷（铝暴露组：130±7%，n = 9；铝暴露 + Vit E组：129±4%，n = 8；P > 0.05）没有显著影响；（2）铝处理也降低了EPSP LTD（对照组：84±4%，n = 7；铝暴露组：92±7%，n = 9，P < 0.01）和PS LTD（对照组：81±4%，n = 7；铝暴露组：98±5%，n = 9，P < 0.001）的幅度。Vit E处理对受损的EPSP LTD（铝暴露组：92±7%，n = 9；铝暴露 + Vit E组：9