Dopamine, a reward signal in the brain, can retroactively convert hippocampal synaptic depression into potentiation, suggesting an elegant biological solution to the distal reward problem.

Dopamine transporter (DAT) interaction with furopyrimidine called AIM-100 in intact cells leads to dramatic oligomerization, nanoclustering and endocytosis of DAT by a novel mechanism coupled to the transporter molecule conformation.

Dopamine signaling is necessary for normal fear extinction learning.

Attenuated anticipatory activity in ventromedial prefrontal cortex is modulated by dopamine D1 receptor density in nucleus accumbens, and accounts for impaired probabilistic reward learning in older adults.

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

Rat behavior and dopamine release are preferentially modulated by subjective rather than objective evaluation of outcomes in a social setting.

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

Discrimination of predictive and non-predictive fear stimuli requires plasticity in the lateral amygdala that is regulated by midbrain dopamine neurons.

Inhibiting ventral tegmental dopamine neurons, or their inputs to nucleus accumbens, disrupts cue-motivated reward seeking in a manner that depends on the microstructure of behavior.

Dopamine novelty signals are localized in the posterior tail of the striatum along with general salience signals, while dopamine in the ventral striatum reliably encodes reward prediction error.