Wang M, Chen J -T, Ruan D -Y, Xu Y -Z
School of Life Science, University of Science and Technology of China, Hefei, Anhui 230027, PR China.
Neuroscience. 2002;113(2):411-9. doi: 10.1016/s0306-4522(02)00193-8.
Previous studies from our group have demonstrated that chronic aluminum exposure from parturition throughout life impairs both long-term potentiation (LTP) and long-term depression (LTD) of the excitatory postsynaptic potential (EPSP) slope and reduces the population spike (PS) amplitude in the rat dentate gyrus in vivo. The present study sought to extend these findings by evaluating the developmental periods critical for aluminum-induced impairment of synaptic plasticity. Rats were exposed to aluminum (gestational, lactational and postlactational) through drinking 0.3% aluminum chloride in water over different developmental intervals: (1) prenatal exposure; (2) beginning from birth and terminating at weaning; (3) beginning at weaning throughout life; (4) beginning at birth and continuing throughout life. As adults (postnatal day 80-100), field potentials were measured in the dentate gyrus of hippocampus in response to stimulation applied to the lateral perforant path. The results showed: (1) Prenatal aluminum exposure had no effect on the magnitude of LTP as measured by the EPSP slope and LTD as measured for the PS amplitude, while it had a small effect on the magnitude of LTP as measured for the PS amplitude and LTD as measured by the EPSP slope. (2) Lactational, postlactational and throughout life exposure to aluminum impaired both LTP and LTD of the EPSP slope and PS amplitude, except that LTD of PS amplitude was not significantly changed in animals postlactationally exposed. (3) Aluminum exposure from parturition throughout life caused the greatest impairment of the range of synaptic plasticity, while prenatal aluminum exposure caused the least. From these results we conclude that the lactational period was the most susceptible to aluminum-induced impairment of synaptic plasticity and that chronic aluminum exposure from parturition throughout life is extremely disruptive to synaptic plasticity and should be avoided.
我们小组之前的研究表明,从分娩开始终生慢性铝暴露会损害兴奋性突触后电位(EPSP)斜率的长时程增强(LTP)和长时程抑制(LTD),并降低大鼠齿状回体内群体峰电位(PS)的幅度。本研究旨在通过评估对铝诱导的突触可塑性损害至关重要的发育时期来扩展这些发现。大鼠在不同发育阶段通过饮用含0.3%氯化铝的水暴露于铝(孕期、哺乳期和哺乳期后):(1)产前暴露;(2)从出生开始到断奶结束;(3)从断奶开始直至终生;(4)从出生开始并持续终生。成年后(出生后第80 - 100天),测量海马齿状回对施加于外侧穿通路径的刺激的场电位。结果显示:(1)产前铝暴露对以EPSP斜率测量的LTP幅度和以PS幅度测量的LTD幅度没有影响,而对以PS幅度测量的LTP幅度和以EPSP斜率测量的LTD幅度有轻微影响。(2)哺乳期、哺乳期后和终生暴露于铝会损害EPSP斜率和PS幅度的LTP和LTD,除了哺乳期后暴露的动物中PS幅度的LTD没有显著变化。(3)从分娩开始终生铝暴露对突触可塑性范围的损害最大,而产前铝暴露造成的损害最小。从这些结果我们得出结论,哺乳期对铝诱导的突触可塑性损害最敏感,并且从分娩开始终生慢性铝暴露对突触可塑性极具破坏性,应予以避免。