Early life adversity (ELA), defined as an adverse experience during critical periods in brain development, is a risk factor for neurodevelopmental and psychiatric disorders. The major effector molecules of stress are glucocorticoids (GCs), which by binding to glucocorticoid receptors (GRs) regulate several biological processes in the brain and the body. So far, little is known about the effects of ELA on a subtype of glial cells, named oligodendrocyte precursor cells (OPCs) or NG2-glia. To investigate how GCs can affect the molecular signature of the NG2-glia and impact the behavioral phenotype in mice, we generated a mouse strain with a conditional knockout (cKO) of the GR in NG2-glia. We used a combination of immunohistochemistry and fluorescence-activated cell sorting to characterize this mouse strain and found a significant reduction of the GR in OPCs. Furthermore, the cKO of GR in NG2-glia affected oligodendrocyte differentiation, resulting in reduced mature oligodendrocytes in adult cKO mice. In behavioral tests, cKO mice displayed impairment in learning and memory tasks compared to wild-types. The limited bedding and nesting (LBN) paradigm will be used to induce stress in pups through fragmented maternal care. Preliminary results indicate that an early cKO of GR in NG2-glia affects oligodendrocyte differentiation and behavioral outcome later in life, thus suggesting a role of GCs on the OPCs-mediated neural circuit refinement. Deciphering the role of the GR on OPCs during ELA could give an insight into the mechanisms contributing to the development of stress-related disorders and potentially lead to novel pharmacological targets.