Astrocytes are the most abundant glial cell type in the central nervous system. They express G-protein-coupled receptors (GPCRs), which respond to inflammatory and stress mediators. Activation of astrocytic GPCRs triggers elevation in intracellular calcium levels and the production and release of astrocytic factors. These astrocytic factors play crucial roles in modulating synapse numbers and synaptic plasticity.Changes in synapse numbers have been documented in neurodevelopmental disorders (NDDs). Many epidemiological studies indicate that chronic inflammation and stress during critical neurodevelopmental periods influence the onset NDDs. Notably, the primary visual cortex V1 emerges as one of the most significantly impacted brain region, displaying changes in both gene and protein expression (including GPCRs). Similarly, alterations in visual plasticity have been reported. Nevertheless, the precise role of astrocytes in these alterations remains elusive.We aimed to investigate if astrocyte abnormal over-activation during V1 critical neurodevelopmental period is sufficient to induce, a posteriori in young adulthood, NDD-like altered defects in visual synaptic plasticity.To address this aim, the DREADD technology was combined to in vivo electrophysiology. We found that chronic astrocytic activation alters long-lasting plasticity and visual memory in young adult mice. Our study holds promise in understanding better the role of astrocytes in the development of NDDs.