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.
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.
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