Abstract
BackgroundPost-traumatic stress disorder (PTSD) is an anxious disorder associated with low levels of corticosterone and enhanced negative feedback of the hypothalamic–pituitary–adrenal (HPA) axis. Previous studies showed that the amygdala not only has an excitatory effect on the HPA axis but also plays a key role in fear-related behaviors. Coticosterone exert actions through binding to the mineralocorticoid (MR) and glucocorticoid receptor (GR), which are abundant in the amygdala. In our previous study, down-regulation of MR and GR in the hippocampus of PTSD rats was found. But the roles of MR and GR in the amygdala of PTSD rats is incompletely understood.Resultswistar rats were divided into 1 d, 7 d, 14 d groups after single prolonged stress (SPS) and control group. SPS is a reliable animal model of PTSD. Open field test (OF) and elevated plus maze tests (EPM) were performed to examine fear-related behaviors. Morphological changes of the ultrastructure of the amygdala neurons were assessed by transmission electron microscopy (TEM). Dual-immunofluorescence histochemistry was used to determined subcellular distribution and colocalization of MR- and GR-ir. Protein and mRNA of MR and GR was examined by western blotting and RT-PCR. OF and EPM showed enhanced fear in SPS rats. Abnormal neuronal morphology was discovered in the amygdala of SPS rats. The expression of MR- and GR-ir intensity, mRNA and protein within the amygdala decreased after SPS at 1 day, and then gradually recovered by 14 days, although the degree of decrease and recovery were different amongst techniques. We found no change in the MR/GR ratio at 3 levels of the amygdala. But more cytoplasmic distribution and decreased colocalization of MR- and GR-ir were observed in the amygdala after 7 days of SPS.ConclusionThese data suggest that change of MR and GR in the amygdala are involved in the mechanisms of fear in PTSD.
Highlights
Post-traumatic stress disorder (PTSD) is an anxious disorder associated with low levels of corticosterone and enhanced negative feedback of the hypothalamic–pituitary–adrenal (HPA) axis
Post-traumatic stress disorder (PTSD) is an anxiety disorder that develops after exposure to a life-threatening traumatic experience, and is characterized by intrusive memories, a hyper-arousal state and avoidance of stimuli associated with the trauma [1]
Rats showed a significant reduction in time spent in the central area (*P < 0.05) as well as a reduction in the number of central squares crossed at 1 day, 7 days and 14 days after single prolonged stress (SPS) exposure in comparison with control group
Summary
Post-traumatic stress disorder (PTSD) is an anxious disorder associated with low levels of corticosterone and enhanced negative feedback of the hypothalamic–pituitary–adrenal (HPA) axis. PTSD is characterized by changes in the neuroendocrine system including abnormal blood corticosteroid concentration and enhanced negative feedback of the hypothalamic–pituitary–adrenal (HPA) axis [2,3]. Unbound MR and GR are believed to be primarily localized in the cytoplasm, but can translocate to the nucleus after binding to the hormone ligand. Both receptors show different affinity for corticosteroids; MR has a higher affinity for corticosteroids than the GR [4,5]. At basal levels of corticosterone, MR is believed to be predominant in the maintenance of homeostasis, whereas GR becomes activated when corticosteroid levels increase after stress [3]
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