Invertebrate gamma-aminobutyric acid-gated chloride channel

Invertebrate gamma-aminobutyric acid-gated chloride channels are ligand-gated ion channels that mediate fast synaptic inhibition in the nervous system of insects and other invertebrates[2]. When the neurotransmitter GABA binds to these pentameric channels, they open to allow chloride ions to flow into the neuron, hyperpolarizing the membrane and inhibiting neural activity. These channels are the molecular targets of several important classes of insecticides—including cyclodienes, phenylpyrazoles, and isoxazolines—which either antagonize or allosterically modulate channel function to disrupt normal neuronal signaling, ultimately causing paralysis or death in pest insects. A canonical invertebrate subunit is RDL, widely studied in Drosophila and other insects. Mutations in these channels are a major mechanism by which insects develop resistance against GABAergic insecticides[2]. They are highly conserved in invertebrates and structurally related to, but pharmacologically distinct from, vertebrate GABA-A receptors.

Other names

Invertebrate GABA-gated chloride channelInsect GABA receptor (commonly: RDL, acronym from “resistant to dieldrin” in insects)Ionotropic GABA receptor (in invertebrates)GABA-gated chloride channel (in insects)

Drugs bind to the chloride channel pore or allosteric sites, modulating channel opening, either enhancing (agonists) or blocking (antagonists) chloride influx, thereby inhibiting or disinhibiting neuronal firing[2].