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.

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.

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.

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

Dopamine neurons projecting to different targets receive a similar set of inputs, rather than forming reciprocal connections, whereas those projecting to the posterior striatum receive a distinct set of inputs.

Midbrain dopamine neurons in rats signal discrepancies between predicted and actual rewards, regardless of whether the rewards are predicted on the basis of experience or inference.

Dopamine neurons signal value prediction errors (VPEs) integrating information about both reward and aversion, in low reward contexts, whereas VPEs in some dopamine neurons are distorted in high reward contexts.

The conditional reduction of glutaminase in mouse dopamine neurons selectively attenuates glutamate cotransmission at phasic frequencies, revealing the role of dopamine neuron glutamate cotransmission in the attribution of motivational salience.

When learning the reward probability of novel cues, dopamine neurons convey dissociable value and novelty signals.

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