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

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.

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.

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

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.

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

Chemically distinct opioid ligands promote selective protein recruitment by opioid receptors in intact cells.

The structure-based design established a new approach to control pathway-selective activation of opioid receptors, resulting in new dual MOR/KOR G-protein biased agonist analgesics with attenuated liabilities.

Rats exposed to a single stressful event experience days-long constitutive activation of the kappa opioid receptor at inhibitory synapses in part of the brain’s reward system, which increases their drug-seeking behavior.

Exogenous opioid analgesia is mediated by MORs expressed in glutamatergic neurons, whereas endogenous opioid analgesia is mediated by MORs expressed in GABAergic neurons.