Superoxide Anion-Dependent Mitochondrial Fission Contributes to Hippocampal Synaptic Dysfunction in Stress-Susceptible Mice.

ABSTRACT: Reduced synaptic plasticity of hippocampal neurons is a core aspect of depression. Mitochondrial dysfunction affects the synaptic plasticity of neurons. However, the characteristics and molecular mechanisms of mitochondrial dysfunction in hippocampal neurons remain unclear. Oxidative stress observed in depression suggests that excess superoxide anion radical (O₂ ^•-), the first ROS generated in mitochondria, may play crucial roles in mediating mitochondrial damage associated with depression. Unfortunately, current small-molecule fluorescent probes may suffer from diffusion after reacting with O₂ ^•-, thereby limiting the accuracy of studying O₂ ^•-'s biological roles in subcellular structures. Thus, we exploited a fluorescence

SUBMITTER: Li X 

PROVIDER: S-EPMC12569654 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature