Extrasynaptic GABAA receptors that emerge at puberty trigger adolescent synaptic pruning; pruning is prevented and cognition is impaired if the receptors are absent.
Presynaptic GABAB receptors are highly expressed and strongly suppress synaptic transmission at the input and output of hippocampal somatostatin interneurons.
Differential, state-dependent occupancy of three discrete binding sites on α1β3 GABAA receptors determines whether a specific neurosteroid analogue potentiates or inhibits GABA-elicited currents or competitively antagonizes neurosteroid action.
A novel GABAAR assembly pathway that promotes synaptic inhibition is established and provides a molecular explanation for how GABAARs with distinct subunit compositions display distinct subcellular distributions.
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).
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.