<p>Astrocytes, a major class of glial cells, are critical regulators of neuronal synapse development and function. Deficits in astrocyte-synapse interactions are implicated in various neurological disorders, yet the precise mechanisms by which astrocytes guide synapse formation and maturation during development remain poorly understood. A key astrocytic mechanism for integrating both extrinsic (e.g., neuronal) and intrinsic signals is the IP3-mediated release of intracellular calcium (Ca²⁺) from endoplasmic reticulum (ER) stores, modulating a wide range of downstream effects. Though defects in this signaling pathway have been linked to adult brain dysfunction, its role in shaping synaptic development, a period when astrocyte-neuron communication is established, is largely unknown. Here, we investigate the role of IP3-mediated Ca²⁺ signaling in synapse development in the mouse visual system. Using a combination of histological, molecular, and circuit-level approaches, we find that loss of the IP3 receptor (IP3R type 2; IP3R2) leads to significant deficits in the structural maturation of glutamatergic synapses. These synaptic disruptions are accompanied by attenuated visually evoked neuronal activation and impaired behavioral responses to visual threat stimuli. We further show that astrocytic morphological complexity is diminished in the absence of IP3R2, suggesting that store-released Ca²⁺ is required for the maturation of astrocyte-neuron interactions. Our findings establish a critical role for IP3R2-mediated Ca²⁺ signaling in shaping excitatory circuit development and the emergence of visually driven behaviors.</p>