RESUMEN
Exposure to trauma is a potential contributor to anxiety; however, the molecular mechanisms responsible for trauma-induced anxiety require further clarification. In this study, in an aim to explore these mechanisms, we observed the changes in the hypothalamic pituitary adrenal (HPA) axis using a radioimmunoassay and the changes in anxiety-like behavior using the open field test and elevated plus maze test in a rat model following intervention with NBI27914, a specific corticotropinreleasing hormone receptor 1 (CRHR1) antagonist. CRHR1 was found to be involved in traumainduced anxiety. We then applied bioinformatic analysis to screen microRNAs (miRNAs or miRs) that target CRHR1, and miR34b was determined to negatively regulate CRHR1 mRNA in primary hypothalamic neurons. The overexpression of miR34b in the paraventricular nucleus (PVN) by a miRNA agomir using a drug delivery system decreased the hyperactivity of the HPA axis and anxietylike behavior. Overall, the involvement of the HPA axis in traumainduced anxiety was demonstrated, and trauma-induced anxiety was attenuated by decreasing the hyperactivity of the HPA axis via miR34b by targeting CRHR1.