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

Local brain functional activity reductions in bvFTD follow the distribution of serotonergic, GABAergic, and norepinephrinergic neurotransmitter systems, indicating a selective vulnerability and providing novel insights into the underlying disease mechanisms.

Dimensionality reduction techniques reveal how the organization of neurotransmitter receptor and transporter co-expression in the human brain may bridge the gap between brain structure and function.

GABA-A receptors on dopamine neuron axons not only depolarize the membrane but also limit action potential propagation, an effect potentiated by positive allosteric modulators of GABA-A receptors like diazepam (Valium).

Robust fear learning deficits and decreased tonic activity of NAc cholinergic interneurons caused by depletion of MeCP2 could be attributed to an elevation in α2-containing GABA_A receptors.

APP interacts with KCC2 to limit the latter from tyrosine-phosphorylation and ubiquitination and thus subsequent degradation, revealing a novel molecular pathway in which APP regulates GABAergic signaling and thus inhibition in the hippocampus.

Electrophysiological and simulation approaches show that a chloride-related longer relaxation of the inhibitory synaptic events partially compensates the early defect in the chloride homeostasis detected in fetal SOD spinal motoneurons.

Teneurin-2, a synaptic organizer, localizes to microtubule-rich inhibitory synapses and recruits microtubules via interaction with end-binding proteins, and this mechanism enables GABA_A receptors exocytosis.

Excitatory and inhibitory postsynaptic receptors are maintained at corresponded postsynaptic sites with the different dependency of presynaptic neurons in the mature mammalian brain.

Rats exposed to a single stressful event experience days-long constitutive activation of the kappa opioid receptor at inhibitory synapses in part of the brain’s reward system, which increases their drug-seeking behavior.