Insect gamma-aminobutyric acid-gated chloride channel receptor (RDL)

The insect gamma-aminobutyric acid-gated chloride channel receptor (commonly known as RDL) is a pentameric ligand-gated ion channel that mediates inhibitory neurotransmission in the insect central nervous system[2][5]. Upon binding of GABA, the receptor undergoes a conformational change, allowing chloride ions to flow into the neuron, leading to membrane hyperpolarization and reduced neuronal excitability[1][2]. This receptor is a primary target for several classes of insecticides, including cyclodienes (like dieldrin), phenylpyrazoles (fipronil), and isoxazolines, which act by blocking chloride conductance and thereby causing hyperexcitation and death in insects[1][2][5]. The RDL variant is especially notable for its association with insecticide resistance due to mutations that decrease insecticide binding without majorly impairing receptor function[2][5]. This target remains central in the development of selective insecticides and the study of resistance mechanisms at the molecular level[3][5].

Other names

insect GABA receptorinsect GABA-gated chloride channelinsect GABA receptor chloride channelGABA receptor RDL subunitresistance to dieldrin receptor

Non-competitive antagonism (blockade of chloride conductance); Allosteric modulation (potentiation or inhibition of GABA effect); Orthosteric agonism (GABA binding: receptor activation)