奶油
谷氨酸的
突触
神经毒性
突触可塑性
谷氨酸受体
突触素
生物
突触后密度
脑源性神经营养因子
长时程增强
神经营养因子
神经科学
化学
细胞生物学
内科学
生物化学
医学
毒性
转录因子
免疫学
受体
免疫组织化学
基因
作者
Ziwen An,Jing Yang,Fang Xiao,Junli Lv,Xiaoqing Xing,Heqiong Liu,Lei Wang,Yi Liu,Zhanchi Zhang,Huicai Guo
标识
DOI:10.1021/acs.jafc.3c01344
摘要
Perfluorooctane sulfonate (PFOS), a new type of persistent organic pollutant in the environment of water, has drawn significant attention in recent years due to its widespread prevalence and high toxicity. Neurotoxicity is regarded as one of the major toxic effects of PFOS, while research studies on PFOS-induced depression and the underlying mechanisms remain scarce. In this study, behavioral tests revealed the depressive-like behaviors in PFOS-exposed male mice. Neuron damages including pyknosis and staining deepening were identified through hematoxylin and eosin staining. Then, we noticed the elevation of glutamate and proline levels as well as the decline of glutamine and tryptophan levels. Proteomics analysis identified 105 differentially expressed proteins that change in a dose-dependent manner and revealed that PFOS exposure activated the glutamatergic synapse signaling pathway, which were further confirmed by Western blot, and the data were consistent with the findings of the proteomics analysis. Additionally, the downstream signaling cyclic AMP-responsive element-binding protein (CREB)/brain-derived neurotrophic factor (BDNF) and synaptic plasticity-related postsynaptic density protein 95, synaptophysin, were downregulated. Our results highlight that PFOS exposure may inhibit the synaptic plasticity of the hippocampus via glutamatergic synapse and the CREB/BDNF signaling pathway to cause depressive-like behaviors in male mice.
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