The pleasure of rewards in humans is mediated by an opioidergic mechanism.

Analysis of population diversity of SARS-CoV-2 revealed positive epistasis between sites carrying mutations characterizing rapidly expanding lineages.

Taking advantage of awell-established learning paradigm, conditioned taste aversion (CTA), change of hedonic value of a palatable tastant revealed the neural mechanisms encoding this learning process.

Administration of dopamine and opioid receptor antagonists resulted in reduced reward anticipation (effort and increased negative facial reactions), but only administration of opioid antagonists resulted in reduced liking (facial reactions).

Drosophila experience two hunger states, one driven by need and the other by pleasure, which arise from unique neural substrates.

Dopamine modulates behavioral measures of learning and pleasantness in a learning task guided by intrinsic reward, inducing long-term memory benefits specially in those participants with a high sensitivity to reward.

Blocking input from basolateral amygdala to gustatory cortex (GC) severely reduces the coherence of GC ensemble activity, which negatively affects epochal dynamics involved in driving palatability-driven consumption.

Reducing activation of opioidergic receptors strengthens the communication between control and reward circuits in the brain during hedonic judgements.

A computational model of decision making suggests that the dorsolateral prefrontal cortex's role in self-control is more associated with evidence accumulation processes than with inhibition or modulation of value.

Low effort-based motivation to pursue naturally rewarding stimuli can be increased pharmacologically, by targeting inactivation of a single voltage-gated potassium channel within the mesolimbic dopamine reward system.