Astrocytes are essential components of the tripartite synapse, modulating neuronal communication and plasticity. A key mechanism involves GABA transporter GAT-3, mainly expressed in astrocytes, which terminates GABAergic signaling and preserves homeostasis. Here, we investigated hippocampal GAT-3 in spatial memory dynamics—consolidation, expression, and reconsolidation—using the spatial object recognition (SOR) task in rats. Pharmacological inhibition with SNAP-5114 (SNAP) impaired consolidation. This deficiency was rescued by prior open field (OF) exposure and blocked by the protein synthesis inhibitor emetine, indicating protein synthesis reliance. Pre-treatment with the proteasome inhibitor β-Lactacystin (β-Lacta) also mitigated SNAP-induced deficits. Puromycin incorporation assays confirmed that SNAP reduced hippocampal protein synthesis. Additionally, SNAP before retrieval impaired memory expression, which was restored by OF or β-Lacta. In contrast, SNAP did not affect reconsolidation, a process disrupted instead by a broader GABA transporter blocker: Nipecotic Acid. These findings reveal that astrocytic GAT-3 selectively modulates memory consolidation and expression, but not reconsolidation, through protein synthesis. Thus, GAT-3 emerges as a pivotal astrocytic regulator of memory dynamics and a potential therapeutic target in disorders with altered GABAergic signaling and cognitive decline, such as epilepsy, Alzheimer’s disease, and other neuropsychiatric conditions.