Formaldehyde Impairs Learning and Memory Involving the Disturbance of Hydrogen Sulfide Generation in the Hippocampus of Rats
Formaldehyde Impairs Learning and Memory Involving the Disturbance of Hydrogen Sulfide Generation in the Hippocampus of Rats
复制标题
DOI：
10.1007/s12031-012-9912-4
复制
发表时间：
2012
影响因子：
3.1
通讯作者：
Xiao-Qing Tang;Yuan-Yuan Zhuang-Yuan;Ping Zhang;Heng-Rong Fang;Cheng-fang Zhou;Hong-Feng Gu;Hui Zhang;
中科院分区：
文献类型：
--
作者：
Xiao-Qing Tang;Yuan-Yuan Zhuang-Yuan;Ping Zhang;Heng-Rong Fang;Cheng-fang Zhou;Hong-Feng Gu;Hui Zhang;
甲醛（FA）是一种众所周知的室内和室外污染物，已被认为是神经认知障碍发展的负责人。硫化氢（H2S）是第三种气体转运蛋白，是一种内源性神经调质，可促进海马长时程增强，参与学习记忆功能。本研究观察了侧脑室注射FA对大鼠学习记忆形成及海马内源性H2S生成的影响。结果表明，侧脑室注射FA可明显损害大鼠Morris水迷宫和新物体识别实验中的学习记忆功能，增加海马细胞凋亡和脂质过氧化的形成。我们还发现，FA暴露抑制了海马中负责内源性H2S产生的主要酶胱硫醚β-合成酶的表达，并减少了大鼠海马中内源性H2S的产生。这些结果表明，FA干扰海马内源性H2S的产生，导致氧化应激介导的神经元损伤，最终损害学习和记忆功能。我们的研究结果表明，海马内源性H2S的产生障碍是一个潜在的贡献机制，在FA引起的学习和记忆障碍。
Formaldehyde (FA), a well-known indoor and outdoor pollutant, has been implicated as the responsible agent in the development of neurocognitive disorders. Hydrogen sulfide (H2S), the third gasotransimitter, is an endogenous neuromodulator, which facilitates the induction of hippocampal long-term potentiation, involving the functions of learning and memory. In the present study, we analyzed the effects of intracerebroventricular injection of FA on the formation of learning and memory and the generation of endogenous H2S in the hippocampus of rats. We found that the intracerebroventricular injection of FA in rats impairs the function of learning and memory in the Morris water maze and novel object recognition test and increases the formation of apoptosis and lipid peroxidation in the hippocampus. We also showed that FA exposure inhibits the expression of cystathionine β-synthase, the major enzyme responsible for endogenous H2S generation in hippocampus and decreases the production of endogenous H2S in hippocampus in rats. These results suggested that FA-disturbed generation of endogenous H2S in hippocampus leads to the oxidative stress-mediated neuron damage, ultimately impairing the function of learning and memory. Our findings imply that the disturbance of endogenous H2S generation in hippocampus is a potential contributing mechanism underling FA-caused learning and memory impairment.