Changes in integrin αv, vinculin and connexin43 in the medial prefrontal cortex in rats under single-prolonged stress

Abstract

Post-traumatic stress disorder (PTSD) is a stress-accociated mental disorder that occurs as a result of exposure to a traumatic event, with characteristic symptoms, including intrusive memories, hyperarousal and avoidance. The medial prefrontal cortex (mPFC) is known to be significantly involved in emotional adjustment, particularly introspection, inhibition of the amygdala and emotional memory. Previous structural neuroimaging studies have revealed that the mPFC of PTSD patients was significantly smaller when compared with that of controls and their emotional adjustment function was weakened. However, the mechanisms that cause such atrophy remain to be elucidated. The aim of the present study was to elucidate the possible mechanisms involved in apoptosis induced by single-prolonged stress (SPS) in the mPFC of PTSD rats. SPS is an animal model reflective of PTSD. Of the proposed animal models of PTSD, SPS is one that has been shown to be reliably reproducible in patients with PTSD. Wistar rats were sacrificed at 1, 4, 7 and 14 days after exposure to SPS. Apoptotic cells were assessed using electron microscopy and the TUNEL method. Expression of integrin αv, vinculin and connexin43 were detected using immunohistochemistry, western blotting and reverse transcription polymerase chain reaction. The present results demonstrated that apoptotic cells significantly increased in the mPFC of SPS rats, accompanied with changes in expression of integrin αv, vinculin and connexin43. The present results indicated that SPS-induced apoptosis in the mPFC of PTSD rats and the mitochondrial pathway were involved in the process of SPS-induced apoptosis.

Change of Rin1 and Stathmin in the Animal Model of Traumatic Stresses

“…Enhanced MT function may be required to maintain basic physiological functions of cells under the condition with SPS-induced high apoptosis ratio condition (Hirokawa and Takemura, 2005 ). Changes in cytoskeletal proteins integrin, vinculin and connexin 43 are also found in our previous study (Li et al, 2015 ), which are consistent with increased MTs. Few studies at present have focused directly on stathmin expression in fear-related psychological disorders.…”

Tanshinone IIA improves contextual fear‐ and anxiety‐like behaviors in mice via the CREB/BDNF/TrkB signaling pathway

“…Numerous studies have revealed that hippocampus, amygdala, and medial prefrontal cortex (mPFC) were involved in PTSD modulation (Blouin, Sillivan, Joseph, & Miller, 2016; Bremner, 2006; Li et al, 2015; Malivoire, Girard, Patel, & Monson, 2018). In this study, we focus our research in the hippocampus because this region is crucial for fear, episodic and contextual learning, and memory processes related to PTSD symptomatology (Logue et al, 2018).…”

“…Fear conditioning and sensitization both play crucial roles in PTSD. Conditioned fear and single‐prolonged stress are widely used to establish animal models for PTSD study (Flati et al, 2020; Li, Han, & Shi, 2015). In order to maximally mimic the pathophysiology alterations of PTSD patients, double stress (CF + SPS) was employed to mimic the acute and incident stress, which induces mood disorder, exaggerated fear responses and malignant memory in mice (Wang et al, 2012).…”

Recent advances in the role of miRNAs in post-traumatic stress disorder and traumatic brain injury

“…The deletion of FKBP5 can reduce depression-like phenotype and lead to stress resilience [ 11 , 84 ]. Additionally, the mPFC, amygdala, and hippocampus are all consistently implicated in the occurrence of PTSD, and two subregions of mPFC were found that could control the fear and stress behaviors [ 24 , 85 ].…”