Our results showed that FLX Ruxolitinib treatment partially restored the decrease of neuronal survival and completely reserved the alteration of cell differentiation caused by auditory fear conditioning. Strikingly, FLX treatment suppressed auditory fear memory, although the effects were not observed untill 30–60 days after fear conditioning. The effects of FLX treatment could be attributed to the increased survival of amygdaloid cells and maturation of new-born neurons in the amygdala, perhaps leading to a better adaption to the situation. Hippocampal adult-born neurons functionally integrated into existing local circuits at 4–8 weeks of age. Thirty days after fear conditioning, the newborn neurons in the amygdala were approximately 5-week old and might have been integrated into local circuits, producing more functional plasticity. Chronic FLX administration increases brainderived neurotrophic factor expression in many brain areas, including the amygdala and hippocampus, and BDNF is a major mediator of the adult neurogenesis. Increased BDNF in the amygdala and hippocampus likely contributed to the partially rescue of the fear-conditioning-induced impairment of adult neurogenesis by FLX, but this will require further investigation. A recent report showed that the fear erasure requires FLX treatment combined with extinction training. Our results are consistent with this report, but while FLX suppressed auditory fear memory, the freezing levels in FLX fear rats still higher than that of naı¨ve rats. Adult neurogenesis could enable the dynamic remodeling of mature neuronal circuits by adding new neurons, contributing to structural and functional plasticity in the brain. FLX treatment ameliorated the impairment of amygdaloid neurogenesis aftere fear conditioning, and thus protected plasticity in the amygdala. Our study also showed that the number of adult-born cells in the amygdala reached to peak at 7 days after fear conditioning, and two months after the fear conditioning, only about forty percent of BrdU-positive cells expressing NeuN in the amygdala in control rats, which suggested that adult-born cells in the amygdala have longer proliferation time periods and fewer cells attain a mature phenotype compared to those in the hippocampus. These data could contribute to a new understanding for the treatment of PTSD based on the distinct characteristics of the adult neurogenesis in the amygdala and hippocampus. In the study, we used BrdU to investigate the relationship between amygdaloid neurogenesis and auditory fear memory. BrdU can incorporate DNA of dividing cells during the S-phase of the cell cycle, so not all BrdU-labeled cells are neural cells, which is the limitation of BrdU, through BrdU-labeling is the most used method for studying adult neurogenesis. AcrB is a multidrug transporter in the inner membrane of Escherichia coli.