•  Astrocytes encapsulate GABAergic synapses and express GABAA receptors and GABA transporters. They are tightly coupled by gap junctions, and are referred to as the gap junction‐coupled astrocytic network. •  With higher [Cl−]i, GABA application can mediate bidirectional Cl− fluxes in astrocytes, Cl− efflux via GABAA receptors, and Cl− influx along with GABA uptake via GABA transporters. •  We focused on the Cl− dynamics of the astrocytic network under GABAergic synapse transmission. Spillover of GABA predominantly induced Cl− efflux via GABAA receptors, presumably because they are localized more closely to the synaptic cleft. •  GABAA receptor‐mediated currents were propagated via gap junctions within the astrocytic network. These results indicate that Cl− efflux from astrocytes mediated by GABAergic transmission is homeostatically maintained within gap junction‐coupled astrocytic networks. •  Blockage of gap junctional coupling by octanol promoted the collapse of the driving force for neuronal inhibitory transmission during intense activation of GABAergic synapses. Thus, the astrocytic network may play a role in maintaining GABAergic transmission by regulating [Cl−]o. Abstract  The electrophysiological properties and functional role of GABAergic signal transmission from neurons to the gap junction‐coupled astrocytic network are still unclear. GABA‐induced astrocytic Cl− flux has been hypothesized to affect the driving force for GABAergic transmission by modulating [Cl−]o. Thus, revealing the properties of GABA‐mediated astrocytic responses will deepen our understanding of GABAergic signal transmission. Here, we analysed the Cl− dynamics of neurons and astrocytes in CA1 hippocampal GABAergic tripartite synapses, using Cl− imaging during GABA application, and whole cell recordings from interneuron–astrocyte pairs in the stratum lacunosum‐moleculare. Astrocytic [Cl−]i was adjusted to physiological conditions (40 mm). Although GABA application evoked bidirectional Cl− flux via GABAA receptors and mouse GABA transporter 4 (mGAT4) in CA1 astrocytes, a train of interneuron firing induced only GABAA receptor‐mediated inward currents in an adjacent astrocyte. A GAT1 inhibitor increased the interneuron firing‐induced currents and induced bicuculline‐insensitive, mGAT4 inhibitor‐sensitive currents, suggesting that synaptic spillover of GABA predominantly induced the astrocytic Cl− efflux because GABAA receptors are localized near the synaptic clefts. This GABA‐induced Cl− efflux was accompanied by Cl− siphoning via the gap junctions of the astrocytic network because gap junction inhibitors significantly reduced the interneuron firing‐induced currents. Thus, Cl− efflux from astrocytes is homeostatically maintained within astrocytic networks. A gap junction inhibitor enhanced the activity‐dependent depolarizing shifts of reversal potential of neuronal IPSCs evoked by repetitive stimulation to GABAergic synapses. These results suggest that Cl− conductance within the astrocytic network may contribute to maintaining GABAergic synaptic transmission by regulating [Cl−]o.