Social isolation induces succinate dehydrogenase dysfunction in anxious mice. (December 2022)

• Record Type: Journal Article
• Authors: Watanabe, Saki; Al Omran, Alzahra J.; Shao, Amy S.; Zhang, Zeyu; Xue, Chen; Zhang, Jifeng; Watanabe, Junji; Liang, Jing
• Is Part Of: Neurochemistry international. Volume 161(2022)
• Publication Date: 2022-12
• Subjects: Dihydromyricetin -- Succinate dehydrogenase -- Complex II -- Social isolation -- Anxiety -- Stress; GABAAR gamma-aminobutyric acid (A) receptor -- DHM Dihydromyricetin -- ETC Electron transport chain; Neurochemistry -- Periodicals; Neurochemistry -- Periodicals; Neurochimie -- Périodiques; Neurochemistry; Periodicals; 612.804205
• DOI: 10.1016/j.neuint.2022.105434
• Languages: English
• ISSNs: 0197-0186

Abstract

Abstract: We have previously reported social isolation induces anxiety-like behavior, cognitive decline, and reduction in brain ATP levels in mice. These changes were ameliorated by treatment with dihydromyricetin (DHM), a compound that positively modulates γ-aminobutyric A (GABA A) receptor. To gain further insight into the subcellular mechanisms underlying these changes, we utilized a social isolation-induced anxiety mouse model and investigated changes in mitochondrial oxidative capacity via the electron transport chain. We found that 4 weeks of social isolation decreased ATP levels by 43% and succinate dehydrogenase capacity by 52% of the control, while daily DHM (2 mg/kg oral) administration restored succinate dehydrogenase capacity. These results suggest that social isolation decreased mitochondrial capacity to generate ATP. DHM can be developed to be a therapeutic against anxiety and mitochondrial stress.