Spinal Cord Injury Model Mitochondria Connect Altered Function with Defects of Mitochondrion Morphology: an Ultrastructural Study

The key role of mitochondria in neurodegenerative disease patients is well documented. Recent studies claimed that mitochondrial regulatory dysfunction might play a role in ongoing cell death and dysfunction. In the present study, we characterized ultrastructural morphometry of mitochondrial alterations occurring at the level of motor neuron cell bodies in SCI-induced rats. We applied 17 beta-estradiol (E2) to determine whether it can improve mitochondria structural integrity of motor neurons. We used a rat model of acute SCI generated by spinal cord contusion at the T9-T10 level, followed by tissue processing 21 days post-SCI. Samples were divided into five groups: laminectomy, SCI, vehicle, SCI + 25 mu g/kg E2, and SCI + 10 mu g/kg E2. Assessments included analysis of hind limb motor recovery, quantifying tissue repair, and evaluation of morphological changes in the ultrastructure of mitochondria in motor neurons by transmission electron microscopy. In the E2-treated groups, especially the group receiving 25 mu g/kg E2, less irregular mitochondria were observed, as there was a significant reduction in swelling or vacuolization, or fragmentation compared to the SCI group. Furthermore, E2 significantly reduced membrane rupture in the SCI group. E2 could be a proper therapeutic agent to relieve mitochondrial deleterious effects on neurons in neurodegenerative diseases.

Automated summary

The study investigates the impact of 17 beta-estradiol (E2) on mitochondrial alterations in motor neurons induced by spinal cord injury in rats. The results suggest that E2 treatment can improve mitochondria structural integrity and reduce irregular mitochondrial features in motor neurons.