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Dopamine signaling is necessary for normal fear extinction learning.

Building on previous work (Huang et al., 2016), we show that translational control by p-eIF2α is a defense mechanism that prevents persistent cocaine-induced synaptic synaptic potentiation underlying compulsive drug seeking.

Oxytocin, a peptide linked to the processing of socially meaningful stimuli, modulates excitatory synaptic transmission in dopaminergic neurons of ventral tegmental area via retrograde endocannabinoid signaling, acting as a pathway-specific temporal filter for synaptic inputs.

In vivo deconstruction of reward-related behaviors with circuit and pharmacological specificity using designer, light-controllable nicotinic acetylcholine receptors.

Simultaneous quantification of each of the main motor programs in the roundworm C. elegans yields new insights into the neural mechanisms that coordinate animal behavior.

Risk of punishment during reward seeking behavior is associated with a functional "disconnection" of the PFC-VTA circuit due to a transient loss of VTA-driven theta oscillation.

Some dopaminergic neurons release both dopamine and nitric oxide to increase the flexibility of olfactory memories.

Non-synaptic extracellular vesicles may be involved in the release of endogenous cannabinoids in the central nervous system thereby representing a novel mechanism to mediate their effects on synaptic transmission.

HCN2 channels in the ventral tegmental area play an important role in the pathophysiology of chronic mild stress-induced behavioral deficits.