Most ChAT-expressing interneurons are a subset VIP+ interneurons that differentially release GABA and acetylcholine onto different post-synaptic targets, while a separate population of non-VIP ChAT+ neurons release acetylcholine in mPFC.

Structure of the triheteromeric α1β1γ2S GABAA receptor in complex with GABA illuminates the principles of receptor assembly and agonist binding.

Combining GABA with fMRI measurements in the human brain uncovers distinct suppression mechanisms that optimize perceptual decisions through learning and experience-dependent plasticity in the visual cortex.

Mobile and immobile GABA_A receptors in the C. elegans neuromuscular synapse are stabilized by two distinct protein scaffolds.

The molecular mechanisms by which midbrain dopamine neurons acquire the inhibitory neurotransmitter GABA for synaptic release are revealed.

In the brain at rest, the degree of coordinated activity within the motor network is inversely related to levels of the inhibitory transmitter GABA in primary motor cortex.

Extrasynaptic GABA_A receptors that emerge at puberty trigger adolescent synaptic pruning; pruning is prevented and cognition is impaired if the receptors are absent.

Gab1 is a key downstream effector of PDGF signaling and essential to oligodendrocyte differentiation by linking PDGF signaling with GSK3β/β-catenin module.

Building on previous work (Stagg et al., 2014), it is shown that transcranial direct current stimulation modulates local GABA concentration and functional connectivity in the human motor cortex.

All perisomatic GABAergic synpases on hippocampal pyramidal cells have a similar GABA_A receptor subunit composition.