1College of Life Science, Nankai University, Tianjin, China.
Hum Exp Toxicol. 2014 Feb;33(2):203-13. doi: 10.1177/0960327113494902. Epub 2013 Jul 8.
The aim of the present study was to investigate whether cognitive behavioral impairment, induced by nicotine in offspring rats, was associated with the alteration of hippocampal short-term potentiation (STP) and long-term potentiation (LTP) and to discuss the potential underlying mechanism. Young adult offspring rats were randomly divided into three groups. The groups include: control group (CC), nicotine group 1 (NC), in which their mothers received nicotine from gestational day 3 (GD3) to GD18, and nicotine group 2 (CN), in which young adult offspring rats received nicotine from postnatal day 42 (PD42) to PD56. Morris water maze (MWM) test was performed and then field excitatory postsynaptic potentials elicited by the stimulation of perforant pathway were recorded in the hippocampal dentate gyrus region. The results of the MWM test showed that learning and memory were impaired by either prenatal or postnatal nicotine exposure. In addition, it was found that there was no statistical difference of the MWM data between both nicotine treatments. In the electrophysiological test, LTP and STP were significantly inhibited in both NC and CN groups in comparison with the CC group. Notably, STP in CN group was also lower than that in the NC group. These findings suggested that both prenatal and postnatal exposure to nicotine induced learning and memory deficits, while the potential mechanism might be different from each other due to their dissimilar impairments of synaptic plasticity.
本研究旨在探讨尼古丁诱导的子代大鼠认知行为损伤是否与海马体短期增强（STP）和长期增强（LTP）的改变有关，并探讨潜在的机制。将年轻成年子代大鼠随机分为三组：对照组（CC）、尼古丁组 1（NC），其母鼠从妊娠第 3 天（GD3）至第 18 天（GD18）接受尼古丁；尼古丁组 2（CN），其年轻成年子代大鼠从出生后第 42 天（PD42）至第 56 天（PD56）接受尼古丁。通过 Morris 水迷宫（MWM）测试，然后在海马齿状回区域记录由穿通通路刺激引起的场兴奋性突触后电位。MWM 测试的结果表明，产前或产后尼古丁暴露均可损害学习和记忆能力。此外，发现两种尼古丁处理之间的 MWM 数据没有统计学差异。在电生理测试中，NC 和 CN 组的 LTP 和 STP 与 CC 组相比均受到显著抑制。值得注意的是，CN 组的 STP 也低于 NC 组。这些发现表明，产前和产后暴露于尼古丁均可导致学习和记忆缺陷，而由于突触可塑性的损伤不同，其潜在机制可能彼此不同。
