[Alteration of apoptosis and Akt/mTOR signal pathway in hippocampal neurons of rat with post-traumatic stress]

Sichuan Da Xue Xue Bao Yi Xue Ban. 2014 Mar;45(2):221-4.
[Article in Chinese]

Abstract

Objective: To observe the changes of apoptosis and protein kinase B/the mammalian target of Rapamycin (Akt/mTOR) signal pathway in hippocampal neurons of rat with post-straumatic stress disorder (PTSD), and to investigate the mechanism of PTSD.

Methods: Sixty male adult SD rats were divided into control group (n = 10) and PTSD (n = 50) model group. The PTSD animal model was established by giving the rats single-prolonged stress followed a single inescapable electric foot shock (SPS & S). The neuronal apoptosis of hiappocampus of PTSD rats at 1 d, 4 d, 7 d, 14 d and 28 d after model established was detected by flow cytometry (FCM). The expressions of phosphatase and tensin homology deleted on chromosome Ten (PTEN), phosphorylation of ARt and mTOR (p-Akt and p-mTOR) protein were detected by Western blotting.

Results: The apoptotic cell rate in PTSD 1 d, 4 d, 7 d and 14 d rats were higher than that in control rats (P < 0.05). The PTEN expression level was higher since PTSD 1 d than that in control group, and peaked in PTSD 4 d (P < 0.05). The p-Akt expression level was lower in PTSD 1 d than that in control group, and then increased in various time points after PTSD, but it was still lower in PTSD 28 d (P < 0.05). The p-mTOR expression level was lower than that in control group since PTSD 4 d, and then increased in various time points after PTSD 4 d, but it was still lower in PTSD 28 d (P < 0.05).

Conclusion: The Akt/mTOR signal pathway was actived in hippocampal neurons of PTSD rats, and which was involved in neuronal apoptosis regulation.

MeSH terms

  • Animals
  • Apoptosis*
  • Disease Models, Animal
  • Hippocampus / cytology
  • Male
  • Neurons / cytology*
  • Neurons / pathology
  • PTEN Phosphohydrolase / metabolism
  • Phosphorylation
  • Proto-Oncogene Proteins c-akt / metabolism*
  • Rats
  • Rats, Sprague-Dawley
  • Signal Transduction*
  • Stress Disorders, Post-Traumatic / physiopathology*
  • TOR Serine-Threonine Kinases / metabolism*

Substances

  • mTOR protein, rat
  • Proto-Oncogene Proteins c-akt
  • TOR Serine-Threonine Kinases
  • PTEN Phosphohydrolase
  • Pten protein, rat