Component of a heterodimeric G-protein coupled receptor for GABA, formed by gbb-1 and gbb-2 (By similarity). Within the heterodimeric GABA receptor, only gbb-1 seems to bind agonists, while gbb-2 mediates coupling to G proteins (By similarity). Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of down-stream effectors, such as adenylate cyclase (By similarity). Signaling inhibits adenylate cyclase, stimulates phospholipase A2, activates potassium channels, inactivates voltage-dependent calcium-channels and modulates inositol phospholipid hydrolysis (By similarity). Plays a critical role in the fine-tuning of inhibitory synaptic transmission (By similarity). Pre-synaptic GABA receptor inhibits neurotransmitter release by down-regulating high-voltage activated calcium channels, whereas postsynaptic GABA receptor decreases neuronal excitability by activating a prominent inwardly rectifying potassium (Kir) conductance that underlies the late inhibitory postsynaptic potentials (By similarity). Along with gbb-1, may couple to the G(o)-alpha G-protein goa-1 to negatively regulate cholinergic receptor activity in the presence of high levels of acetylcholine in ventral cord motor neurons (PubMed:18614679). As acetylcholine depolarizes body wall muscles, modulation of acetylcholine levels most likely results in the control of locomotory behavior (PubMed:18614679). Regulates locomotory behavior in response to GABA release by GABAergic motor neurons (PubMed:18614679, PubMed:21613582). May form a heterodimer with gbb-1. Expressed in cholinergic motor neurons. Alpha-helical parts of the C-terminal intracellular region may mediate heterodimeric interaction with gbb-1. Increased sensitivity to the acetylcholine esterase inhibitor Aldicarb, which results in accelerated paralysis likely due to enhanced acetylcholine release by ventral cord neurons and enhanced depolarization of muscles on one side of the body (PubMed:18614679). Increased locomotion and body curvature (deeper bends) in response to induced GABA release of GABAergic motor neurons, which in wild-type animals results in acute body relaxation (PubMed:21613582). Double knockout with gbb-1 also results in increased sensitivity to Aldicarb and accelerated paralysis, but in addition results in irregular locomotory behavior characterized by increased speed of locomotion, decreased turning frequency, reduced rate of reversals, and an increased maximal distance covered in a 40 second interval (PubMed:18614679). Double knockout with the muscarinic acetylcholine receptor gar-2 results in a slight increase in sensitivity to Aldicarb and accelerated paralysis 50 minutes following exposure to Aldicarb as compared to the gar-2 and gbb-2 single mutants (PubMed:18614679). Double knockout with the GABA(A) receptor unc-49 results in body elongation defects in response to induced GABA release of GABAergic motor neurons (PubMed:21613582). Belongs to the G-protein coupled receptor 3 family.