Category: receptor_pharmacology
GABA-B receptors are the metabotropic arm of GABAergic inhibition: obligate heterodimers of GABA-B1 (ligand-binding) and GABA-B2 (G-protein-coupling) subunits that signal through Gαi/o. Unlike the ionotropic GABA-A receptor (a ligand-gated Cl⁻ channel; see gaba_a_receptor_signaling), GABA-B produces slower, longer-lasting inhibition via two effector arms — presynaptic suppression of P/Q- and N-type Ca²⁺ channels that dampens neurotransmitter release (auto- and heteroreceptors), and postsynaptic activation of GIRK/Kir3 K⁺ channels that generates the slow IPSP — both reinforced by adenylate-cyclase inhibition that lowers cAMP/PKA tone. Clinically, the orthosteric agonist baclofen treats spasticity; phenibut and γ-hydroxybutyrate (sodium oxybate) are weaker/partial GABA-B agonists with additional targets. These ligands appear in gaba_a_receptor_signaling only as mechanistic contrast; this pathway is their primary home.