Recent evidence suggests that manipulation of astrocytic GqPCR can alter animal behavior related to learning and memory through modulation of neuronal functions. It has been shown that impairment of GqPCR-mediated Ca²⁺ signaling in astrocytes and/or gliotransmitter release causes depression-like behaviors in mice. However, it is not clear whether astrocytic GqPCR signaling is a target for driving behavior related to stress and motivation. We focused on the ventral hippocampus (vHIP), which contributes to stress and depression, and investigated the effect of chemogenetic manipulation of astrocytic GpPCR signaling in animal behavior related to stress. We expressed hM3Dq, a Gq-DREADD, selectively in astrocytes in the vHIP by injecting AAV bilaterally. Activation of hM3Dq caused robust Ca²⁺ elevation in astrocytes and modulated synaptic transmission. Astrocytic GpPCR activation did not alter place preference assessed by open filed test, suggesting no increase in fear-related behavior. Chronic but not acute administration of hM3Dq agonist decreased immobility time in the tail suspension test. These results suggest that chronic activation of GqPCR signaling in vHIP astrocytes should enhance active coping in response to stress and chemogenetic manipulation of astrocytic Ca²⁺ signaling in the vHIP may enhance resilience to stress.