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.

The subcortical visual pathway through the midbrain superior colliculus is responsible for visually evoked Pavlovian conditioning and dopamine neuron responses with predicted value in monkeys, which remained after lesioning V1.

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.

Dopamine neurons function as an ensemble to signal a multidimensional feature prediction error.

Dopamine neurons make novel glutamatergic connections to striatal cholinergic interneurons in the lateral dorsal striatum that are mediated by metabotropic glutamate receptors coupled to TrpC channels.

For mice, knowing when it is time to feed is dependent on the neurotransmitter dopamine and the D1R receptor of neurons in the dorsal striatum.

Dopamine neurons in medial versus lateral VTA encode different signals during fear extinction, yet inhibition of both populations influences fear extinction, at different times.

Disinhibition of dopamine neurons in the midbrain drives heroin reinforcement, the initial step towards opioid addiction.

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

Despite the fundamental relationship between movement and value, they are represented in a separable manner in dopamine neurons.