Abstract <p>Early life stress (ELS) induces long-term changes in neuroplasticity,which are associated with oxytocinergic system dysfunction. However,the molecular mechanisms of these impairments and the possibilitiesfor their correction remain insufficiently studied. This work investigatedthe influence of ELS, exogenous oxytocin (OXT), and the oxytocinreceptor antagonist atosiban on cellular processes related to homeostasisand neurogenesis in neurospheres in vitro. Neurospheres were isolatedfrom the subventricular zone and piriform cortex of CD1 mouse brains(age P60) from control and ELS groups, followed by oxytocin (1 µM)or atosiban (1 µM) treatment. The levels of apoptosis, the degreeof DNA damage (γH2AX), and the expression of neurogenesis markergenes <i>PSA-NCAM</i>, <i>Dcx</i>, <i>Tbr1</i>, <i>Gad67</i>, and <i>Vglut1</i> werequantified using qRT-PCR. It was found that ELS increased the levelof cell apoptosis and decreased the expression of <i>PSA-NCAM</i>, <i>Dcx</i>,and <i>Gad67</i> genes, while oxytocinled to a decrease in the number of apoptotic cells but did not affectthe expression of the studied genes, except for the suppressionof <i>Tbr1</i>. In control cultures,oxytocin increased the expression of <i>PSA-NCAM</i> and <i>Tbr1</i>, while simultaneously reducingthe level of <i>Gad67</i>, which mayreflect a regulatory influence of this gene on the balance of excitatoryand inhibitory transmission in the developing neuronal network.Atosiban-induced stimulation, in turn, led to increased apoptosisin control samples, emphasizing the role of oxytocinergic activityin maintaining neuronal viability even in the absence of stressfactors. The obtained data indicate that ELS causes long-term impairmentsin neurogenesis and cellular homeostasis, while the modulating effectof OXT relies on the initial state of cells. These results highlightthe potential role of the oxytocinergic system in correcting theconsequences of ELS.</p>