Chen J, Wang M, Ruan D, She J
School of Life Science, University of Science and Technology of China, P.O. Box 4, Hefei, Anhui 230027, China.
Neuroscience. 2002;112(4):879-87. doi: 10.1016/s0306-4522(02)00138-0.
As an important neurotoxin, aluminium can cause cognitive dysfunctions and mental diseases. Previous studies have reported that aluminium impaired long-term potentiation (LTP) in vivo and in vitro. Here, we utilise two models of synaptic plasticity, LTP and long-term depression (LTD) to study the effects of aluminium on synaptic plasticity in vivo. Neonatal Wistar rats were chronically exposed to aluminium from birth to weaning via the milk of dams fed with 0.3% aluminium chloride solution. Excitatory postsynaptic potential (EPSP) and population spikes (PS) were recorded from the dentate gyrus (DG) of adult rats by electrically stimulating the perforant path. THE FOLLOWING RESULTS WERE OBTAINED: (1) The input/output function indicated that, as compared to controls, aluminium increased the baseline amplitude of the PS, but decreased the baseline slope of EPSP. (2) Aluminium significantly prevented LTD in PS (controls: 77.36+/-6.7%, n=7; aluminium-exposed: 102.01+/-9.1%, n=7; P<0.05) and decreased the LTD amplitude in EPSP (controls: 76.61+/-4.1%, n=7; aluminium-exposed: 94.31+/-7.9% n=7, P<0.05). (3) Aluminium reduced the amplitude of LTP in both PS (controls: 190+/-16.1%, n=7; aluminium-exposed: 135+/-9.7%, n=7; P<0.05) and EPSP (control: 132+/-9.3%, n=7; aluminium-exposed: 115+/-10.6%, n=7; P<0.05). As for LTD and LTP, PS was impaired more seriously than EPSP in aluminium-exposed rats. (4) Aluminium exposure decreased the paired-pulse facilitation (PPF) of PS at 30-150 ms interpulse interval (IPI), and reduced 93.5% of PPF at 80 ms IPI in PS (controls: 243.4+/-39.8%, n=7; aluminium-exposed: 149.9+/-12.3%, n=7). There was no significant difference in EPSP of PPF. From these results we conclude that aluminium exposure in neonatal rats thus reduces the amplitude of LTP and PPF and blocks the induction of LTD in the DG. We suggest that aluminium affects both presynaptic and postsynaptic mechanisms of synaptic transmission.
作为一种重要的神经毒素，铝可导致认知功能障碍和精神疾病。先前的研究报道，铝在体内和体外均可损害长时程增强（LTP）。在此，我们利用两种突触可塑性模型，即LTP和长时程抑制（LTD）来研究铝对体内突触可塑性的影响。新生Wistar大鼠从出生到断奶通过喂食含0.3%氯化铝溶液的母鼠乳汁长期暴露于铝中。通过电刺激穿通通路，记录成年大鼠齿状回（DG）的兴奋性突触后电位（EPSP）和群体峰电位（PS）。获得以下结果：（1）输入/输出功能表明，与对照组相比，铝增加了PS的基线幅度，但降低了EPSP的基线斜率。（2）铝显著阻止了PS中的LTD（对照组：77.36±6.7%，n = 7；铝暴露组：102.01±9.1%，n = 7；P<0.05），并降低了EPSP中的LTD幅度（对照组：76.61±下4.1%，n = 7；铝暴露组：94.31±7.9%，n = 7，P<0.05）。（3）铝降低了PS（对照组：190±16.1%，n = 7；铝暴露组：135±9.7%，n = 7；P<0.05）和EPSP（对照组：132±9.3%，n = 7；铝暴露组：115±10.6%，n = 7；P<0.05）中LTP的幅度。至于LTD和LTP，在铝暴露大鼠中，PS比EPSP受损更严重。（4）铝暴露降低了PS在30 - 150 ms脉冲间隔（IPI）时的双脉冲易化（PPF），并在PS中使80 ms IPI时的PPF降低了93.5%（对照组：243.4±39.8%，n = 7；铝暴露组：149.9±12.3%，n = 7）。EPSP的PPF无显著差异。从这些结果我们得出结论，新生大鼠暴露于铝中会降低LTP和PPF的幅度，并阻断DG中LTD的诱导。我们认为铝影响突触传递的突触前和突触后机制。
Zotero 插件