Soluble amyloid-β precursor peptide has no functional effects at recombinant and native GABA_B receptors.

A critical regulator of inhibitory neurotransmitter signaling in the hippocampus has been identified in experiments on mice and been shown to play essential role in synaptic plasticity and memory.

The direct interaction of R-type Ca²⁺ channel Cav2.3 and GABA_B receptor auxiliary subunits in the active zone of medial habenula terminals scales synaptic strength independent of GABA_B receptor activation.

Presynaptic GABAB receptors are highly expressed and strongly suppress synaptic transmission at the input and output of hippocampal somatostatin interneurons.

Single bouton measurements of calcium influx shows that activating GABA_B receptors at nerve terminals can lead to complete inhibition of calcium entry when one is operating at the physiological setpoint of extracellular calcium concentration.

Functional analysis reveals a distinct mode of action of the allosteric modulators in the GABA_B receptor in a pocket that is formed only in the active state and identifies a region in the GABA_B2 subunit important for allosteric agonism.

The sodium leak NALCN channel functions as a core effector of GABA-B and D2 receptors that is used along with GIRK channels to regulate action potential firing in dopamine neurons.

Summation of metabotropic GABAergic responses remain linear even if most superficial layer interneurons specialized to recruit GABA_B receptors are simultaneously active.

Purkinje cell collaterals regulate processing in the input layer of the cerebellum by providing fast stochastic GABA_A-mediated and slow GABA_B-mediated inhibition to a specialized subset of unipolar brush cells.

A multi-scale integration of experimental and computational approaches shows how a non-linear dependence of T-type calcium channel gating on GABA_B receptor activity regulates thalamic network oscillations.