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.

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

Neurons of the cholinergic system, which release the excitatory neurotransmitter acetycholine throughout the cortex, also release the inhibitory transmitter GABA, with potential implications for cognitive function.

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.

Functional identification of GABAergic neurons in the ventral tegmental area as a important neuronal subpopulation regulating non-rapid eye movement (NREM) sleep in mice.

Experiments examining the actions of morphine on single neurons from one of the brain's reward centers, the VTA, reveal the mechanism by which the drug exerts its hedonic effects.

A seasonal switch to excitatory GABAA signaling dictates how daily clock neurons interact to encode environmental change.

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.

A chemical screen reveals that a compound used to treat a parasitic disease can trigger pluripotent stem cells to become neurons, uncovering a novel mechanism behind neuronal development.

The activity of a set of GABAergic neurons is causally linked with a locomotory pattern in moving animals, and the mechanisms underlying the neuromodulatory role of GABA are illuminated.