Opioids stop breathing during overdose by silencing two small brain sites, with just 140 neurons in the breathing rhythm generator exerting the key effect.

Quantitative imaging of neurons reveals how opioid agonists produce long-term functional tolerance at presynaptic terminals through rapid internalization of receptors from the axonal surface.

Activation of mu-opioid receptors in the nucleus accumbens by their endogenous ligands promotes consumption of high-fat food in sated but not hungry rats, via enhancement of a neural signal that promotes cued approach behavior.

Corticospinal functional MRI reveals that the opioid remifentanil and the level of perceived analgesia modulate coupling strength between the prefrontal cortex, brainstem, and spinal cord.

Attention-grabbing tasks produce rapid opioid-mediated analgesia via the descending pain modulation network to alter spinal neuronal activity.

Pro-nociceptive and pro-inflammatory TRPM3 (transient receptor potential melastatin 3) channels, expressed in somatosensory neurons, are inhibited by activation of Gαi-coupled receptors, such as µ-opioid receptors, in vitro and in vivo.

The discovery that opioid neuropeptide neuronal signaling controls feeding behavior in a genetically tractable invertebrate model may help unravel the mechanisms of appetite control in humans.

Emerging approaches in larval zebrafish to identify safe opioid therapies without the side-effect of respiratory depression.

The key mechanism for opioid-like biased agonists to provide analgesia but not respiratory depression does not involve ß-arrestin 2.

By differentially modulating the two major excitatory inputs to the striatum, mu- and delta-opioid receptors regulate the balance between thalamic and cortical inputs to the striatum.