title: Nitrogen dioxide (NO(2)) pollution as a potential risk factor for developing vascular dementia and its synaptic mechanisms.
abstract: Recent epidemiological literatures reported that NO(2) is a potential risk factor of ischemic stroke in polluted area. Meanwhile, our previous in vivo study found that NO(2) could delay the recovery of nerve function after stroke, implying a possible risk of vascular dementia (VaD) with NO(2) inhalation, which is often a common cognitive complication resulting from stroke. However, the effect and detailed mechanisms have not been fully elucidated. In the present study, synaptic mechanisms, the foundation of neuronal function and viability, were investigated in both model rats of ischemic stroke and healthy rats after NO(2) exposure. Transmission electron microscope (TEM) observation showed that 5 mg m(-3) NO(2) exposure not only exacerbated the ultrastructural impairment of synapses in stroke model rats, but also induced neuronal damage in healthy rats. Meantime, we found that the expression of synaptophysin (SYP) and postsynaptic density protein 95 (PSD-95), two structural markers of synapses in ischemic stroke model were inhibited by NO(2) inhalation; and so it was with the key proteins mediating long-term potentiation (LTP), the major form of synaptic plasticity. On the contrary, NO(2) inhalation induced the expression of nearly all these proteins in healthy rats in a concentration-dependent manner. Our results implied that NO(2) exposure could increase the risk of VaD through inducing excitotoxicity in healthy rats but weakening synaptic plasticity directly in stroke model rats.
authors.affiliation: College of Environment and Resource, Center of Environmental Science and Engineering, Shanxi University, Taiyuan, Shanxi 030006, PR China. lihongyan_xinyue@yahoo.com.cn
authors.forename: Hongyan
authors.initials: H
authors.lastname: Li
authors.forename: Xiaoyun
authors.initials: X
authors.lastname: Xin
mesh_terms: D000393:Air Pollutants / Q000737:chemistry / Q000633:toxicity*; D000818:Animals; D015140:Dementia, Vascular / Q000209:etiology / Q000378:metabolism; D004195:Disease Models, Animal; D000076122:Disks Large Homolog 4 Protein; D006624:Hippocampus / Q000502:physiology; D047908:Intracellular Signaling Peptides and Proteins / Q000378:metabolism; D008297:Male; D008565:Membrane Proteins / Q000378:metabolism; D009473:Neuronal Plasticity / Q000187:drug effects*; D009585:Nitrogen Dioxide / Q000737:chemistry / Q000633:toxicity*; D011494:Protein Kinases / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012307:Risk Factors; D020521:Stroke / Q000378:metabolism / Q000473:pathology; D013569:Synapses / Q000378:metabolism* / Q000648:ultrastructure; D016708:Synaptophysin / Q000378:metabolism; D014157:Transcription Factors / Q000378:metabolism
chemical_list: D000393:Air Pollutants; D000076122:Disks Large Homolog 4 Protein; C501449:Dlg4 protein, rat; D047908:Intracellular Signaling Peptides and Proteins; D008565:Membrane Proteins; D016708:Synaptophysin; D014157:Transcription Factors; D011494:Protein Kinases; D009585:Nitrogen Dioxide