Abstract
A large number of aerospace practices have confirmed that the aerospace microgravity environment can lead to cognitive function decline. Mitochondria are the most important energy metabolism organelles, and some studies demonstrate that the areospace microgravity environment can cause mitochondrial dysfunction. However, the relationships between cognitive function decline and mitochondrial dysfunction in the microgravity environment have not been elucidated. In this study, we simulated the microgravity environment in the Sprague-Dawley (SD) rats by -30° tail suspension for 28 days. We then investigated the changes of mitochondrial morphology and proteomics in the hippocampus. The electron microscopy results showed that the 28-day tail suspension increased the mitochondria number and size of rat hippocampal neuronal soma. Using TMT-based proteomics analysis, we identified 163 differentially expressed proteins (DEPs) between tail suspension and control samples, and among them, 128 proteins were upregulated and 35 proteins were downregulated. Functional and network analyses of the DEPs indicated that several of mitochondrial metabolic processes including the tricarboxylic acid (TCA) cycle were altered by simulating microgravity (SM). We verified 3 upregulated proteins, aconitate hydratase (ACO2), dihydrolipoamide S-succinyltransferase (DLST), and citrate synthase (CS), in the TCA cycle process by western blotting and confirmed their differential expressions between tail suspension and control samples. Taken together, our results demonstrate that 28-day tail suspension can cause changes in the morphology and metabolic function of hippocampus mitochondria, which might represent a mechanism of cognitive disorder caused by aerospace microgravity.
Highlights
Long-term space travel would adversely affect human physiology, and the most common detrimental effects include the visually impaired intracranial pressure syndrome, decreased bone density, muscle atrophy, brain functional and structural changes [1, 2]
We studied the influence of simulated microgravity (SM) on the dynamics and morphology of mitochondria in hippocampal neuronal soma using transmission electron microscopy
The number of mitochondria in the SM group was significantly increased compared to the Control group (p
Summary
Long-term space travel would adversely affect human physiology, and the most common detrimental effects include the visually impaired intracranial pressure syndrome, decreased bone density, muscle atrophy, brain functional and structural changes [1, 2]. Animal tail suspension is a classical and useful approach for the microgravity study on Earth for a long time [3–5]. There have been several reports about the impacts of simulated microgravity (SM) on brain cognitive function. Lin et al demonstrated that SM inhibits the proliferation of adult hippocampal neural stem cells in rats, which maybe the reason of detrimental effects of SM on learning and memory [6]. Our previous research found that tail suspension can damage the learning and memory ability of rats, and the molecules involved in glutamate excitotoxicity and several neurotransmitters (5-hydroxytryptamine, dopamine, γ-amino acid butyric acid and epinephrine) are downregulated [5, 8]
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