comparison the hippocampal stathmin and tfeb proteins level in animal models of ptsd and depression

Background: extensive evidence demonstrates that neuronal autophagic and cytoskeletal elements play critical roles in neuroplasticity. dysregulation of neuroplasticity has been implicated in the pathology of depression and post-traumatic stress disorder (ptsd). transcription factor eb (tfeb) and stathmin are key regulators of autophagy and microtubule formation, respectively. objectives: the current study aimed to compare the levels of hippocampal tfeb and stathmin proteins in ptsd and depressed animal models of rats. methods: three groups of male rat pups (n = 8) were used. the first group, designated as the depressed group, was exposed to maternal separation stress and related stressors. the second group, representing the ptsd model, was exposed to single-prolonged stress. the third group served as the control. anxiety-like and depressive-like behaviors were evaluated using the elevated plus maze (epm) and forced swimming test (fst). hippocampal tfeb and stathmin protein levels were measured using western blotting. data were analyzed using prism software. one-way anova and post hoc tukey tests were performed to evaluate statistical differences between groups in behavioral tasks. independent t-tests were used to assess differences in protein levels between groups. results: the tfeb protein levels were increased in both ptsd and depressed rats, while stathmin levels were decreased. the effect of depression on tfeb expression was significantly higher than in ptsd. conversely, stathmin reduction was more pronounced in ptsd compared to depressed rats. conclusions: these results suggest that changes in stathmin and tfeb protein levels may be associated with anxiety- and depression-like behaviors.