Social isolation induces succinate dehydrogenase dysfunction in anxious mice

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 gamma-aminobutyric A (GABAA) receptor. To gain further insight into the sub -cellular 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 thera-peutic against anxiety and mitochondrial stress.

Automated summary

Social isolation leads to anxiety, cognitive decline, and reduced ATP levels in mice. Treatment with DHM can ameliorate these changes by restoring mitochondrial capacity to generate ATP.