title: Chronic asthma results in cognitive dysfunction in immature mice.
abstract: Asthma is the most common chronic childhood illness today. However, little attention is paid for the impacts of chronic asthma-induced hypoxia on cognitive function in children. The present study used immature mice to establish ovalbumin-induced chronic asthma model, and found that chronic asthma impaired learning and memory ability in Morris Water Maze test. Further study revealed that chronic asthma destroyed synaptic structure, impaired long-term potentiation (LTP) maintaining in the CA1 region of mouse hippocampal slices. We found that intermittent hypoxia during chronic asthma resulted in down-regulation of c-fos, Arc and neurogenesis, which was responsible for the impairment of learning and memory in immature mice. Moreover, our results showed that budesonide treatment alone was inadequate for attenuating chronic asthma-induced cognitive impairment. Therefore, our findings indicate that chronic asthma might result in cognitive dysfunction in children, and more attention should be paid for chronic asthma-induced brain damage in the clinical therapy.
authors: Jiangsu Key Laboratory of Neurodegeneration, Department of Pharmacology, Nanjing Medical University, 140 Hanzhong Road, Nanjing, Jiangsu 210029, China.
authors: Ruo-Bing
authors: RB
authors: Guo
authors: Pei-Li
authors: PL
authors: Sun
authors: An-Peng
authors: AP
authors: Zhao
authors: Jun
authors: J
authors: Gu
authors: Xu
authors: X
authors: Ding
authors: Jun
authors: J
authors: Qi
authors: Xiu-Lan
authors: XL
authors: Sun
authors: Gang
authors: G
authors: Hu
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D001249:Asthma / Q000097:blood / Q000139:chemically induced / Q000150:complications* / Q000188:drug therapy; D001993:Bronchodilator Agents / Q000627:therapeutic use; D019819:Budesonide / Q000627:therapeutic use; D002908:Chronic Disease; D003072:Cognition Disorders / Q000209:etiology* / Q000517:prevention & control; D003598:Cytoskeletal Proteins / Q000378:metabolism; D002658:Developmental Disabilities / Q000209:etiology* / Q000517:prevention & control; D004195:Disease Models, Animal; D005260:Female; D018507:Gene Expression Regulation, Developmental / Q000187:drug effects / Q000502:physiology; D006624:Hippocampus / Q000187:drug effects / Q000503:physiopathology / Q000648:ultrastructure; D066298:In Vitro Techniques; D019394:Ki-67 Antigen / Q000378:metabolism; D008168:Lung / Q000473:pathology / Q000648:ultrastructure; D018782:Maze Learning / Q000187:drug effects; D051379:Mice; D008807:Mice, Inbred BALB C; D009419:Nerve Tissue Proteins / Q000378:metabolism; D010047:Ovalbumin / Q000009:adverse effects; D011014:Pneumonia / Q000188:drug therapy / Q000209:etiology; D013997:Time Factors; D042461:Vascular Endothelial Growth Factor A / Q000097:blood
chemical_list: D001993:Bronchodilator Agents; D003598:Cytoskeletal Proteins; D019394:Ki-67 Antigen; D009419:Nerve Tissue Proteins; D042461:Vascular Endothelial Growth Factor A; C092069:activity regulated cytoskeletal-associated protein; D019819:Budesonide; D010047:Ovalbumin
keywords: Asthma; BALF; Children; DG; G protein-coupled receptor 124; GAPDH; GPR124; HE; HFS; HIF-1α; IEG; LTP; Learning and memory; MWM; Morris Water Maze; PFA; Synaptic plasticity; VEGF; bronchial alveolar lavage fluid; dentate gyrus; fEPSP; field excitatory postsynaptic potential; glyceraldehyde-3-phosphate dehydrogenase; hematoxylin and eosin; high-frequency stimulation; hypoxia induced factor 1α; immediate early gene; long-term potentiation; paraformaldehyde; vascular endothelial growth factor