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Posttraumatic stress disorder (PTSD) is a psychiatric disorder that may lead to a series of changes in the central nervous system, including impaired synaptic plasticity, neuronal dendritic spine loss, enhanced apoptosis and increased inflammation. However, the specific mechanism of PTSD has not been studied clearly. In the present study, we found that the level of miR-153-3p in the hippocampus of rats exposed tosingle-prolonged stresss (SPS) was upregulated, but its downstream target σ-1R showed a significant decrease. The downregulation of miR-153 could alleviate the PTSD-like behaviors in the rats exposed to SPS, and this effect might be related to the upregulation of σ-1R and PSD95. Furthermore, anti-miR-153 could also increase the dendritic spine density and reduce cell apoptosis in the hippocampus of SPS rats. In addition, we showed that the mTOR signaling pathway might be involved in the regulation of σ-1R in the hippocampus of rats exposed to SPS. The results of this study indicated that miR-153 might alleviate PTSD-like behaviors by regulating cell morphology and reducing cell apoptosis in the hippocampus of rats exposed to SPS by targeting σ-1R, which might be related to the mTOR signaling pathway. • The level of miR-153 was upregulated in the hippocampus of rats exposed to SPS procedure, while the level of sigma-1R was downregulated. • Anti-miR-153 injection alleviated PTSD-like behaviors and this effect might be related to the upregulation of PSD95, the decreased level of apoptosis, and the increased density of dendritic spines in hippocampal neurons. • The effect of anti-miR-153 on neurons might be related to its target gene sigma-1R, which activates mTOR signal pathway. [ABSTRACT FROM AUTHOR]