| Autor: |
Kondashevskaya MV; A.P. Avtsyn Research Institute of Human Morphology, B.V. Petrovsky National Research Center of Surgery, Moscow 119991, Russia., Mikhaleva LM; A.P. Avtsyn Research Institute of Human Morphology, B.V. Petrovsky National Research Center of Surgery, Moscow 119991, Russia., Artem'yeva KA; A.P. Avtsyn Research Institute of Human Morphology, B.V. Petrovsky National Research Center of Surgery, Moscow 119991, Russia., Aleksankina VV; A.P. Avtsyn Research Institute of Human Morphology, B.V. Petrovsky National Research Center of Surgery, Moscow 119991, Russia., Areshidze DA; A.P. Avtsyn Research Institute of Human Morphology, B.V. Petrovsky National Research Center of Surgery, Moscow 119991, Russia., Kozlova MA; A.P. Avtsyn Research Institute of Human Morphology, B.V. Petrovsky National Research Center of Surgery, Moscow 119991, Russia., Pashkov AA; Scientific and Educational Center 'Biomedical Technologies', School of Medical Biology, South Ural State University, Chelyabinsk 454080, Russia.; Federal Neurosurgical Center, Novosibirsk 630048, Russia., Manukhina EB; Department of Physiology and Anatomy, University of North Texas Health Science Center, Fort Worth, TX 76107, USA.; Institute of General Pathology and Pathophysiology, Moscow 125315, Russia., Downey HF; Department of Physiology and Anatomy, University of North Texas Health Science Center, Fort Worth, TX 76107, USA., Tseilikman OB; Scientific and Educational Center 'Biomedical Technologies', School of Medical Biology, South Ural State University, Chelyabinsk 454080, Russia.; Faculty of Basic Medicine, Chelyabinsk State University, Chelyabinsk 454080, Russia., Yegorov ON; Faculty of Basic Medicine, Chelyabinsk State University, Chelyabinsk 454080, Russia., Zhukov MS; A.P. Avtsyn Research Institute of Human Morphology, B.V. Petrovsky National Research Center of Surgery, Moscow 119991, Russia., Fedotova JO; Laboratory of Neuroendocrinology, Pavlov Institute of Physiology, Saint Petersburg 199034, Russia., Karpenko MN; Department of Physiology, Pavlov Institute of Experimental Medicine, Saint Petersburg 197376, Russia., Tseilikman VE; Scientific and Educational Center 'Biomedical Technologies', School of Medical Biology, South Ural State University, Chelyabinsk 454080, Russia.; Zelman Institute of Medicine and Psychology, Novosibirsk State University, Novosibirsk 630090, Russia. |
| Abstrakt: |
PTSD is associated with disturbed hepatic morphology and metabolism. Neuronal mitochondrial dysfunction is considered a subcellular determinant of PTSD, but a link between hepatic mitochondrial dysfunction and hepatic damage in PTSD has not been demonstrated. Thus, the effects of experimental PTSD on the livers of high anxiety (HA) and low anxiety (LA) rats were compared, and mitochondrial determinants underlying the difference in their hepatic damage were investigated. Rats were exposed to predator stress for 10 days. Then, 14 days post-stress, the rats were evaluated with an elevated plus maze and assigned to HA and LA groups according to their anxiety index. Experimental PTSD caused dystrophic changes in hepatocytes of HA rats and hepatocellular damage evident by increased plasma ALT and AST activities. Mitochondrial dysfunction was evident as a predominance of small-size mitochondria in HA rats, which was positively correlated with anxiety index, activities of plasma transaminases, hepatic lipids, and negatively correlated with hepatic glycogen. In contrast, LA rats had a predominance of medium-sized mitochondria. Thus, we show links between mitochondrial dysfunction, hepatic damage, and heightened anxiety in PTSD rats. These results will provide a foundation for future research on the role of hepatic dysfunction in PTSD pathogenesis. |
