Fig. 3.

GA causes neuronal mitochondrial dysfunction. a–c Western blot analysis of mitochondrial iron import protein Mfrn1, mitochondrial fission protein Drp1, and fusion protein Mfn1. A representative image set is presented. Tissues or neurons were lysed and mitochondria were isolated from rat hippocampal neurons (a), rat-pup hippocampus (b), and aged-mouse hippocampus (c). d Mitochondrial morphology. After GA treatment for 6 h, the hippocampal neurons were stained with MitoTracker Red at 37 °C for 30 min and observed under the confocal microscopy at × 600 magnification. Scale bar 10 μm. e Mitochondrial permeability transition pore (mPTP) opening, determined by mitochondrial swelling assay kit with freshly isolated mitochondria. f Mitochondrial membrane potential (MMP) levels. g ATP production. Data are presented as mean ± SEM (n = 6); *p < 0.05 compared with Con group; ^#p < 0.05 compared with the GA (Ket or Sev) group