GABAB receptor

GABA_BRs stimulate the opening of K⁺ channels, specifically GIRKs, which brings the neuron closer to the equilibrium potential of K⁺. This reduces the frequency of action potentials which reduces neurotransmitter release.^{[citation needed]} Thus GABA_B receptors are usually considered as inhibitory receptors.

GABA_B receptors can also function as an excitatory receptor and facilitate neurotransmitter release via increasing the activity of Ca_V2.3 channels.^[3]

GABA_B receptors usually reduces the activity of adenylyl cyclase and Ca²⁺ channels by using G-proteins with G_i/G₀ α subunits.^[4]

GABA_B receptors are involved in behavioral actions of ethanol,^[5][6] gamma-hydroxybutyric acid (GHB),^[7] baclofen,^[8] and possibly in pain.^[9] Recent research suggests that these receptors may play an important developmental role.^[10]

GABA_B receptors are similar in structure to and in the same receptor family with metabotropic glutamate receptors.^[11] There are two subunits of the receptor, GABA_B1 and GABA_B2,^[12] and these appear to assemble as obligate heterodimers in neuronal membranes by linking up by their intracellular C termini.^[11] In the mammalian brain, two predominant, differentially expressed isoforms of the GABA_B1 are transcribed from the Gabbr1 gene, GABA_B(1a) and GABA_B(1b), which are conserved in different species including humans.^[13] This might potentially offer more complexity in terms of the function due to different composition of the receptor.^[13] Cryo-electron microscopy structures of the full length GABA_B receptor in different conformational states from inactive apo to fully active have been obtained. Unlike Class A and B GPCRs, phospholipids bind within the transmembrane bundles and allosteric modulators bind at the interface of GABA_B1 and GABA_B2 subunits.^{[14][15][16][17][18][19][20]}

• GABA receptor
• GABA_A receptor