Abstract
Acute traumatic event exposure is a direct cause of post-traumatic stress disorder (PTSD). Amygdala is suggested to be associated with the development of PTSD. In our previous findings, different activation patterns of GABAergic neurons and glutamatergic neurons in early or late stages after stress were found. However, the neural plastic mechanism underlying the role of basolateral amygdala (BLA) in post-traumatic stress disorder remains unclear. Therefore, this study mainly aimed at investigating time-dependent morphologic and electrophysiological changes in BLA during the development of PTSD. We used single prolonged stress (SPS) procedure to establish PTSD model of rats. The rats showed no alterations in anxiety behavior as well as in dendritic spine density or synaptic transmission in BLA 1 day after SPS. However, 10 days after SPS, rats showed enhancement of anxiety behavior, and spine density and frequency of miniature excitatory and inhibitory postsynaptic currents in BLA. Our results suggested that after traumatic stress, BLA displayed delayed increase in both spinogenesis and synaptic transmission, which seemed to facilitate the development of PTSD.
Highlights
As an intricate anxiety disorder, post-traumatic stress disorder (PTSD) generally occurs after traumatic stress exposure (Galea et al, 2007; Keyes et al, 2013; Scott et al, 2013; Olaya et al, 2015)
The results of elevated plus maze (EPM) and open field test (OFT) were analyzed with two-way Analysis of variance (ANOVA), and we used single prolonged stress (SPS) (SPS, No SPS) and Post-SPS Day (1 day, 10 day) as the between-subject factors
These results showed that rats displayed delayed onset of anxiety-like behaviors after SPS, which were in line with previous findings (Knox et al, 2012a; Fang et al, 2018)
Summary
As an intricate anxiety disorder, post-traumatic stress disorder (PTSD) generally occurs after traumatic stress exposure (Galea et al, 2007; Keyes et al, 2013; Scott et al, 2013; Olaya et al, 2015). SPS paradigm is composed of the following procedures (Bradley et al, 2005): restraint, forced swim in water at 20–24◦C, ether exposure, and stay at homecage undisturbedly for 7 days which is essential for the development of key symptoms of PTSD (Liberzon et al, 1997; Knox et al, 2012b) This model can mimic the symptoms of PTSD in humans, with behavioral changes including increased anxiety (Han et al, 2014; Fang et al, 2018), impaired social interaction and spatial memory (Wen et al, 2016), and disrupted extinction of fear memory (Iwamoto et al, 2007; Fang et al, 2018)
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