Gamma-amino butyric acid (GABA) is the most abundant inhibitory neurotransmitter in the brain. Normal GABA function requires specialized proteins such as biosynthetic enzymes, transporters and receptors. Defects in these proteins can lead to a specific imbalance of GABA neurotransmission and lead to diseases. Recent studies have shown that both GABAergic neurons and glia cells synthesize and release GABA to maintain neural excitatory-inhibitory balance, neuroprotection, among other functions. Both neurons and glia cells express functional metabotropic and ionotropic GABA receptors, however, the role of these GABA receptors in the glia cells is still unknown. Probably the activation of these receptors in glia cells are important for neuron-glia interactions. Here, we use the model organism C. elegans to uncover the function of GABA receptors expressed in the Amsh glia cell and how these regulate the neuron-glia interactions. In particular, we focus on the study of GABAA receptors, UNC-49, LGC-36 and LGC-38, which are inhibitory chlorine-selective channels and how the activation of these receptors regulates the activity of Amsh glia and consequently the regulation of ASH neuron. We found that both GABA receptors in the Amsh glia affect the activity of these glia cells and the response to the octanol in the ASH neuron. In summary, our results show that UNC-49, LGC-36, and LGC-38 express in the Amsh glia could be an important role in the regulation of neuron-glia interaction.