Disturbed inhibitory synaptic transmission has functional impacts on neurodevelopmental and psychiatric disorders. An essential mechanism for modulating inhibitory synaptic transmission is alteration of the postsynaptic abundance of GABA<sub>A</sub>Rs, which are stabilized by postsynaptic scaffold proteins and recruited by presynaptic signals. However, how GABAergic neurons trigger signals to transsynaptically recruit GABA<sub>A</sub>Rs remains elusive. Here, we show that UNC-43/CaMKII functions at GABAergic neurons to recruit GABA<sub>A</sub>Rs and modulate inhibitory synaptic transmission at C. elegans neuromuscular junctions. We demonstrate that UNC-43 promotes presynaptic MADD-4B/Punctin secretion and NRX-1&#
x3b1;/Neurexin surface delivery. Together, MADD-4B and NRX-1&#
x3b1; recruit postsynaptic NLG-1/Neuroligin and stabilize GABA<sub>A</sub>Rs. Further, the excitation of GABAergic neurons potentiates the recruitment of NLG-1-stabilized-GABA<sub>A</sub>Rs, which depends on UNC-43, MADD-4B, and NRX-1. These data all support that UNC-43 triggers MADD-4B and NRX-1&#
x3b1;, which act as anterograde signals to recruit postsynaptic GABA<sub>A</sub>Rs. Thus, our findings elucidate a mechanism for pre- and postsynaptic communication and inhibitory synaptic transmission and plasticity.