Early-life adversity (ELA) is a risk factor for developing neuropsychiatric disorders like depression. The central nucleus of the amygdala (CeA) is a stress-sensitive region of the brain, involved in reward-related behaviors. Recently, we showed that ELA provokes anhedonia-like behaviors in males, mediated by corticotropin-releasing hormone (CRH) overexpression in the CeA. In the paraventricular nucleus of the hypothalamus (PVN), another stress-sensitive brain region, we find that diminished microglial engulfment of excitatory synapses onto CRH+ neurons is a key mechanism that contributes to altered stress responsivity of male mice exposed to ELA. Interestingly, these two stress-sensitive regions of the brain have different developmental timelines, which suggests the possibility of different critical periods for intervention in the CeA compared to the PVN. There may also be sex-specific effects of ELA and different developmental trajectories between the sexes at baseline. Here, we characterized the developmental trajectory of excitatory and inhibitory synapses onto CRH + neurons in the CeA under control and ELA conditions in males and females. To investigate these developmental changes, we induced ELA using limited bedding and nesting from postnatal days (P)2-10. We employed male and female single-reporter mice (CRH-tdTomato+), in conjunction with immunohistochemistry to label pre- and post- synaptic excitatory and inhibitory puncta. We find that ELA increases excitatory and decreases inhibitory synaptic inputs onto CeA-CRH+ neurons at P14 in males, but not females. This effect in excitatory synapses has been shown to persist until at least P24 in males, and preliminary data shows a trend for decreased numbers of inhibitory synapses in males as well. Ongoing work is examining the long-term excitatory and inhibitory synaptic changes on CRH+ neurons at the adolescent time point of P45. Future directions will include examining microglia-mediated engulfment of excitatory and inhibitory synaptic puncta to pinpoint the peak of synaptic pruning by microglia in the CeA.