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[Effects of hyperoxia on the expression of hippocampal N-methyl D-aspartate receptor 1 and its synapse-associated molecules in neonatal rats]. | LitMetric

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Article Abstract

Objectives: To investigate the effects of hyperoxia on the expression of N-methyl-D-aspartate receptor 1 (NMDAR1) and its synapse-associated molecules, including cannabinoid receptor 1 (CB1R), postsynaptic density 95 (PSD95), and synapsin (SYN), in the hippocampus of neonatal rats.

Methods: One-day-old Sprague-Dawley neonatal rats were randomly divided into a hyperoxia group and a control group (=8 per group). The hyperoxia group was exposed to 80% ± 5% oxygen continuously, while the control group was exposed to room air, for 7 days. At 1, 3, and 7 days after hyperoxia exposure, hematoxylin and eosin (HE) staining was used to observe histopathological changes in the brain. The expression levels of NMDAR1, CB1R, PSD95, and SYN proteins and mRNAs in the hippocampus were detected by immunohistochemistry, Western blotting, and quantitative real-time PCR.

Results: After 7 days of hyperoxia exposure, the hyperoxia group showed decreased neuronal density and disordered arrangement in brain tissue. Compared with the control group, after 1 day of hyperoxia exposure, CB1R mRNA and both NMDAR1 and CB1R protein expression in the hyperoxia group were significantly downregulated, while SYN protein expression was significantly upregulated (<0.05). After 3 days, mRNA expression of NMDAR1, CB1R, and SYN was significantly decreased (<0.05); NMDAR1 and CB1R protein expression was significantly downregulated (<0.05), while PSD95 and SYN protein expression was significantly upregulated (<0.05). After 7 days of hyperoxia, the protein expression of NMDAR1 and CB1R was significantly upregulated (<0.05).

Conclusions: Continuous hyperoxia exposure induces time-dependent changes in the expression levels of NMDAR1 and its synapse-associated molecules in the hippocampus of neonatal rats.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC12369529PMC
http://dx.doi.org/10.7499/j.issn.1008-8830.2501086DOI Listing

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